首页 > 最新文献

Biochimie最新文献

英文 中文
Controlled CRISPR/Cas12a activation via DNAzyme-mediated splitting of chimeric substrate for lead detection. 通过dnazyme介导的嵌合底物分裂控制CRISPR/Cas12a激活用于铅检测。
IF 3 Pub Date : 2026-02-02 DOI: 10.1016/j.biochi.2026.02.001
Peiying Zhang, Meng Shen, Lihua Ding, Leiliang He, Yongjun Wu, Songcheng Yu

Chronic lead exposure poses severe threats to human health, which demands a rapid detection strategy beyond conventional instrumentation-dependent approaches. While CRISPR/Cas12a systems offer promising alternatives through trans-cleavage activity, conventional Pb2+ biosensors relying on DNAzyme-generated intact activators suffer from high background signals due to interference from uncleaved substrates. To address this limitation, we developed a steric-hindrance-controlled activation strategy by employing a chimeric DNAzyme substrate (Sub) that prevents Cas12a binding until Pb2+-dependent cleavage occurs. This DNAzyme-mediated splitting releases two fragments (A1/A2) that rearrange into split activators, triggering the CRISPR/Cas12a trans-cleavage of a quenched reporter (6-FAM/BHQ1). Under the optimal condition, the sensor achieved a linear detection range of 2.5-25 μM (R2 = 0.998) with 2.18 μM LOD and high selectivity against interferents. Validation in tap water matrices demonstrated 98.6%-102.6% recovery (RSD 3.0%-7.5%), which showed robustness in real samples. This split-activator design paradigm eliminates background from uncleaved substrates without additional pretreatment steps to provide a versatile template for converting metal ions into CRISPR-detectable signals.

慢性铅暴露对人类健康构成严重威胁,这需要一种超越传统仪器依赖方法的快速检测战略。虽然CRISPR/Cas12a系统通过反式裂解活性提供了有希望的替代方案,但传统的Pb2+生物传感器依赖于dnazyme生成的完整激活剂,由于未裂解底物的干扰,会受到高背景信号的影响。为了解决这一限制,我们开发了一种空间位阻控制的激活策略,通过使用嵌合DNAzyme底物(Sub)阻止Cas12a结合,直到Pb2+依赖性切割发生。这种dnazyme介导的分裂释放两个片段(A1/A2),它们重新排列成分裂激活因子,触发被猝灭的报告基因(6-FAM/BHQ1)的CRISPR/Cas12a反式切割。在最佳条件下,传感器的线性检测范围为2.5 ~ 25 μM (R2 = 0.998), LOD为2.18 μM,对干扰具有较高的选择性。自来水基质的验证回收率为98.6% ~ 102.6% (RSD为3.0% ~ 7.5%),在实际样品中具有稳健性。这种分裂激活剂设计范例消除了未裂解底物的背景,无需额外的预处理步骤,为将金属离子转化为crispr可检测信号提供了通用模板。
{"title":"Controlled CRISPR/Cas12a activation via DNAzyme-mediated splitting of chimeric substrate for lead detection.","authors":"Peiying Zhang, Meng Shen, Lihua Ding, Leiliang He, Yongjun Wu, Songcheng Yu","doi":"10.1016/j.biochi.2026.02.001","DOIUrl":"10.1016/j.biochi.2026.02.001","url":null,"abstract":"<p><p>Chronic lead exposure poses severe threats to human health, which demands a rapid detection strategy beyond conventional instrumentation-dependent approaches. While CRISPR/Cas12a systems offer promising alternatives through trans-cleavage activity, conventional Pb<sup>2+</sup> biosensors relying on DNAzyme-generated intact activators suffer from high background signals due to interference from uncleaved substrates. To address this limitation, we developed a steric-hindrance-controlled activation strategy by employing a chimeric DNAzyme substrate (Sub) that prevents Cas12a binding until Pb<sup>2+</sup>-dependent cleavage occurs. This DNAzyme-mediated splitting releases two fragments (A1/A2) that rearrange into split activators, triggering the CRISPR/Cas12a trans-cleavage of a quenched reporter (6-FAM/BHQ1). Under the optimal condition, the sensor achieved a linear detection range of 2.5-25 μM (R<sup>2</sup> = 0.998) with 2.18 μM LOD and high selectivity against interferents. Validation in tap water matrices demonstrated 98.6%-102.6% recovery (RSD 3.0%-7.5%), which showed robustness in real samples. This split-activator design paradigm eliminates background from uncleaved substrates without additional pretreatment steps to provide a versatile template for converting metal ions into CRISPR-detectable signals.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":"1-6"},"PeriodicalIF":3.0,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
High oral doses of vitamin B12 in early pregnancy improve B12 status of mother and child irrespective of subsequent supplementation a longitudinal study in B12 insufficient Indian women supplemented with either milk, vitamin pills, or placebo. 妊娠早期高剂量口服维生素B12可改善母亲和孩子的维生素B12状况,无论随后是否补充。一项对维生素B12不足的印度妇女进行的纵向研究,她们分别补充了牛奶、维生素片或安慰剂。
IF 3 Pub Date : 2026-01-30 DOI: 10.1016/j.biochi.2026.01.014
Sadanand Naik, Sergey N Fedosov, Namita Mahalle, Sharwari Narawade, Ebba Nexo, Christian W Heegaard

B12 deficiency during pregnancy has been associated with shunted growth, neural tube defects, anemia, and neuro-cognitive disorders. The optimal prevention strategy remains to be found. Here we explore the effect of high doses of oral B12 in early pregnancy followed by physiological doses of B12 or placebo. The women (B12 < 146 pmol/l) were recruited before week 17 and divided into three groups, all primed for 14 days with oral B12 = 5 mg/day. Then onwards, the participants daily received 400 ml of milk (HO-B12 = 1.6 μg; n = 31), B12-pills (CN-B12 = 1.6 μg; n = 32), or placebo (n = 13) until 4 months postpartum. Blood was drawn at baseline, ½ - 6 months after baseline; on the day of delivery (including cord blood); and at 4-month postpartum (child and mother). B12 status was assessed by measuring plasma B12, holotranscobalamin (holoTC), and homocysteine (Hcy). Birth parameters were recorded. Comparable changes were achieved following high dose administration of both B12-forms. Plasma total B12 and holoTC increased 2-3 and 6-10 times, respectively; while total Hcy decreased ≈2-fold. No clear difference was observed during and after interventions with milk, pills and placebo (including newborns). At the end of the study ⅞ of mothers and ⅔ of babies had adequate B12 status despite its steady downward drift. Our study demonstrates the benefit of an early-stage supplementation to pregnant women with high oral B12. A continuous low dose supplementation adds only minor advantages. The results may impact future strategies of ensuring a sufficient B12 supply during pregnancy.

怀孕期间缺乏B12与发育分流、神经管缺陷、贫血和神经认知障碍有关。最佳的预防策略仍有待寻找。在这里,我们探讨了高剂量口服B12在怀孕早期的影响,然后生理剂量的B12或安慰剂。女性(B1212=5毫克/天)然后,参与者每天服用400毫升牛奶(HO-B12=1.6 μg, n=31), b12药片(CN-B12=1.6 μg, n=32)或安慰剂(n=13),直到产后4个月。在基线后½- 6个月时抽血;分娩当日(含脐带血);产后4个月(孩子和母亲)。通过测定血浆B12、全反钴胺素(holoTC)和同型半胱氨酸(Hcy)来评估B12状态。记录出生参数。在高剂量给药两种b12形式后取得了类似的变化。血浆总B12和holoTC分别升高2 ~ 3倍和6 ~ 10倍;总Hcy降低约2倍。在母乳、药片和安慰剂干预期间和之后(包括新生儿)没有观察到明显的差异。在研究结束时,尽管维生素B12水平稳步下降,但仍有1 / 4的母亲和1 / 3的婴儿有足够的维生素B12水平。我们的研究表明,早期补充维生素B12对口服维生素B12含量高的孕妇有益。持续的低剂量补充只能带来很小的好处。结果可能会影响未来确保怀孕期间充足的B12供应的策略。
{"title":"High oral doses of vitamin B<sub>12</sub> in early pregnancy improve B<sub>12</sub> status of mother and child irrespective of subsequent supplementation a longitudinal study in B<sub>12</sub> insufficient Indian women supplemented with either milk, vitamin pills, or placebo.","authors":"Sadanand Naik, Sergey N Fedosov, Namita Mahalle, Sharwari Narawade, Ebba Nexo, Christian W Heegaard","doi":"10.1016/j.biochi.2026.01.014","DOIUrl":"10.1016/j.biochi.2026.01.014","url":null,"abstract":"<p><p>B<sub>12</sub> deficiency during pregnancy has been associated with shunted growth, neural tube defects, anemia, and neuro-cognitive disorders. The optimal prevention strategy remains to be found. Here we explore the effect of high doses of oral B<sub>12</sub> in early pregnancy followed by physiological doses of B<sub>12</sub> or placebo. The women (B<sub>12</sub> < 146 pmol/l) were recruited before week 17 and divided into three groups, all primed for 14 days with oral B<sub>12</sub> = 5 mg/day. Then onwards, the participants daily received 400 ml of milk (HO-B<sub>12</sub> = 1.6 μg; n = 31), B<sub>12</sub>-pills (CN-B<sub>12</sub> = 1.6 μg; n = 32), or placebo (n = 13) until 4 months postpartum. Blood was drawn at baseline, ½ - 6 months after baseline; on the day of delivery (including cord blood); and at 4-month postpartum (child and mother). B<sub>12</sub> status was assessed by measuring plasma B<sub>12</sub>, holotranscobalamin (holoTC), and homocysteine (Hcy). Birth parameters were recorded. Comparable changes were achieved following high dose administration of both B<sub>12</sub>-forms. Plasma total B<sub>12</sub> and holoTC increased 2-3 and 6-10 times, respectively; while total Hcy decreased ≈2-fold. No clear difference was observed during and after interventions with milk, pills and placebo (including newborns). At the end of the study ⅞ of mothers and ⅔ of babies had adequate B<sub>12</sub> status despite its steady downward drift. Our study demonstrates the benefit of an early-stage supplementation to pregnant women with high oral B<sub>12</sub>. A continuous low dose supplementation adds only minor advantages. The results may impact future strategies of ensuring a sufficient B<sub>12</sub> supply during pregnancy.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The regulation characterization of novel transcription regulator JTY_2262 in Mycobacterium bovis BCG. 新型转录调控因子jty2262在牛分枝杆菌BCG中的调控特性
IF 3 Pub Date : 2026-01-29 DOI: 10.1016/j.biochi.2026.01.013
Jinmiao Song, Hui Wang, Mingrui Sun, Mei Li, Yang Zhang, Jiayin Xing, Shuxian Wang, Ren Fang, Xiaotian Li, Siguo Liu, Zhaoli Li, Ningning Song

Mycobacterium tuberculosis (Mtb) can survive for a long time in vivo and evade host immune attacks, primarily through transcriptional regulation mediated by transcription regulators. JTY_2262 (homologous with Rv2250c) belongs to the Tetracycline Repressor (TetR) family of regulators, and its function is currently unclear. In this study, we combined JTY_2262 overexpressed transcriptomics and electrophoretic mobility shift assays (EMSA) to identify novel targets regulated by JTY_2262. The cofactors containing Cys, VC, VB1, VB3, VB6, Pb2+, Cu2+ and Li + inhibit the binding between JTY_2262 and the JTY_2045 (homologous with rv2031c) promoter. Overall, this study demonstrates that JTY_2262 is a versatile regulator. Under different environmental conditions, JTY_2262 senses concentration variations of specific cofactors. By modulating its DNA-binding affinity accordingly, JTY_2262 regulates targeted gene expression, enabling bacteria to adapt their metabolic machinery and physiological state to better adapt the changing environment.

结核分枝杆菌(Mycobacterium tuberculosis, Mtb)主要通过转录调节剂介导的转录调控,在体内存活较长时间并逃避宿主免疫攻击。JTY_2262(与Rv2250c同源)属于四环素抑制因子(TetR)家族,其功能目前尚不清楚。在这项研究中,我们结合JTY_2262过表达的转录组学和电泳迁移转移测定(EMSA)来鉴定JTY_2262调节的新靶点。含有Cys、VC、VB1、VB3、VB6、Pb2+、Cu2+和Li+的辅助因子抑制JTY_2262与JTY_2045(与rv2031c同源)启动子的结合。总体而言,本研究表明JTY_2262是一种多功能调节剂。在不同的环境条件下,JTY_2262可以感知特定辅因子的浓度变化。jty2262通过相应调节其dna结合亲和力,调控目标基因的表达,使细菌能够调整其代谢机制和生理状态,更好地适应不断变化的环境。
{"title":"The regulation characterization of novel transcription regulator JTY_2262 in Mycobacterium bovis BCG.","authors":"Jinmiao Song, Hui Wang, Mingrui Sun, Mei Li, Yang Zhang, Jiayin Xing, Shuxian Wang, Ren Fang, Xiaotian Li, Siguo Liu, Zhaoli Li, Ningning Song","doi":"10.1016/j.biochi.2026.01.013","DOIUrl":"10.1016/j.biochi.2026.01.013","url":null,"abstract":"<p><p>Mycobacterium tuberculosis (Mtb) can survive for a long time in vivo and evade host immune attacks, primarily through transcriptional regulation mediated by transcription regulators. JTY_2262 (homologous with Rv2250c) belongs to the Tetracycline Repressor (TetR) family of regulators, and its function is currently unclear. In this study, we combined JTY_2262 overexpressed transcriptomics and electrophoretic mobility shift assays (EMSA) to identify novel targets regulated by JTY_2262. The cofactors containing Cys, V<sub>C</sub>, V<sub>B1</sub>, V<sub>B3</sub>, V<sub>B6</sub>, Pb<sup>2+</sup>, Cu<sup>2+</sup> and Li <sup>+</sup> inhibit the binding between JTY_2262 and the JTY_2045 (homologous with rv2031c) promoter. Overall, this study demonstrates that JTY_2262 is a versatile regulator. Under different environmental conditions, JTY_2262 senses concentration variations of specific cofactors. By modulating its DNA-binding affinity accordingly, JTY_2262 regulates targeted gene expression, enabling bacteria to adapt their metabolic machinery and physiological state to better adapt the changing environment.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":"29-39"},"PeriodicalIF":3.0,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The aryl hydrocarbon receptor: A modulator of skeletal muscle health and aging. 芳烃受体:骨骼肌健康和衰老的调节剂。
IF 3 Pub Date : 2025-12-29 DOI: 10.1016/j.biochi.2025.12.012
Keon Wimberly, Terence E Ryan

Skeletal muscle is fundamental to human health, serving as the primary effector of movement and a central regulator of systemic metabolism. Age-related declines in muscle mass and mitochondrial function contribute to frailty, metabolic dysfunction, and loss of independence in older adults. While these changes are often attributed to reduced physical activity, chronic inflammation, and impaired regenerative capacity, emerging evidence implicates environmental and metabolic sensing pathways in muscle degeneration. The aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor best known for mediating responses to environmental pollutants such as dioxins, has recently been recognized as a key regulator of endogenous metabolic and redox processes. AHR activation occurs not only through xenobiotic exposure but also via endogenous ligands derived from tryptophan metabolism-including kynurenine and indole derivatives-whose levels rise in aging, chronic kidney disease (CKD), and other pollutant exposures. Sustained AHR activation in skeletal muscle has been shown to impair mitochondrial oxidative phosphorylation, promote proteolysis, and disrupt neuromuscular junction integrity, linking AHR signaling to muscle pathology. Experimental studies in rodent models demonstrate that pharmacologic or genetic inhibition of AHR can preserve muscle mass, mitochondrial function, and regenerative capacity. This review summarizes the molecular biology of the AHR, its emerging roles in skeletal muscle physiology and pathology, and the growing experimental toolkit for interrogating its function. Understanding how AHR signaling integrates environmental, metabolic, and aging cues may reveal new therapeutic opportunities to preserve skeletal muscle health and physical function across the lifespan.

骨骼肌是人体健康的基础,是运动的主要效应器和全身代谢的中枢调节剂。与年龄相关的肌肉质量和线粒体功能下降会导致老年人身体虚弱、代谢功能障碍和独立性丧失。虽然这些变化通常归因于体力活动减少、慢性炎症和再生能力受损,但新出现的证据表明,环境和代谢感知途径与肌肉变性有关。芳烃受体(AHR)是一种配体激活的转录因子,以介导对环境污染物(如二恶英)的反应而闻名,最近被认为是内源性代谢和氧化还原过程的关键调节因子。AHR激活不仅通过外源暴露发生,还通过色氨酸代谢衍生的内源性配体发生,包括犬尿氨酸和吲哚衍生物,其水平在衰老、慢性肾脏疾病(CKD)和其他污染物暴露中升高。骨骼肌中持续的AHR激活已被证明会损害线粒体氧化磷酸化,促进蛋白质水解,并破坏神经肌肉连接的完整性,将AHR信号与肌肉病理联系起来。啮齿类动物模型的实验研究表明,药物或基因抑制AHR可以保持肌肉质量、线粒体功能和再生能力。本文综述了AHR的分子生物学,其在骨骼肌生理和病理中的新作用,以及越来越多的实验工具来质疑其功能。了解AHR信号如何整合环境、代谢和衰老线索,可能会揭示在整个生命周期中保持骨骼肌健康和身体功能的新治疗机会。
{"title":"The aryl hydrocarbon receptor: A modulator of skeletal muscle health and aging.","authors":"Keon Wimberly, Terence E Ryan","doi":"10.1016/j.biochi.2025.12.012","DOIUrl":"10.1016/j.biochi.2025.12.012","url":null,"abstract":"<p><p>Skeletal muscle is fundamental to human health, serving as the primary effector of movement and a central regulator of systemic metabolism. Age-related declines in muscle mass and mitochondrial function contribute to frailty, metabolic dysfunction, and loss of independence in older adults. While these changes are often attributed to reduced physical activity, chronic inflammation, and impaired regenerative capacity, emerging evidence implicates environmental and metabolic sensing pathways in muscle degeneration. The aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor best known for mediating responses to environmental pollutants such as dioxins, has recently been recognized as a key regulator of endogenous metabolic and redox processes. AHR activation occurs not only through xenobiotic exposure but also via endogenous ligands derived from tryptophan metabolism-including kynurenine and indole derivatives-whose levels rise in aging, chronic kidney disease (CKD), and other pollutant exposures. Sustained AHR activation in skeletal muscle has been shown to impair mitochondrial oxidative phosphorylation, promote proteolysis, and disrupt neuromuscular junction integrity, linking AHR signaling to muscle pathology. Experimental studies in rodent models demonstrate that pharmacologic or genetic inhibition of AHR can preserve muscle mass, mitochondrial function, and regenerative capacity. This review summarizes the molecular biology of the AHR, its emerging roles in skeletal muscle physiology and pathology, and the growing experimental toolkit for interrogating its function. Understanding how AHR signaling integrates environmental, metabolic, and aging cues may reveal new therapeutic opportunities to preserve skeletal muscle health and physical function across the lifespan.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145879733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The antiretroviral drug emtricitabine increases kynurenine: tryptophan ratio, aryl hydrocarbon receptor activation, and cellular senescence in female mice. 抗逆转录病毒药物恩曲他滨增加雌性小鼠犬尿氨酸:色氨酸比例、芳烃受体激活和细胞衰老。
IF 3 Pub Date : 2025-12-28 DOI: 10.1016/j.biochi.2025.12.009
Alok Tripathi, Shabiha Sultana, Sagar Vyavahare, Jie Chen, Arindam Paul, Huidong Shi, Wenbo Zhi, Rafal Pacholczyk, Bharati Mendhe, Apeksha Anand, Anthony Carrillo, Jaeshia Lindsay, Dima W Alhamad, Husam Bensreti, Christopher L Yearwood, Dylan Taylor, Colby Gross, Maribeth Johnson, Eric J Belin de Chantemele, Mark W Hamrick, Meghan E McGee-Lawrence

HIV-associated mortality has been reduced by antiretroviral therapies (ART), but prolonged ART usage by people living with HIV (PLWH) is associated with frailty and poor healthspan. Mechanisms driving this phenomenon are not fully known, but clinical and preclinical studies suggest that HIV and ART may drive aberrant activation of the aryl hydrocarbon receptor (AhR) by kynurenine (KYN), an endogenous metabolite of tryptophan. Therefore, we investigated whether the combination of an HIV-like phenotype (Tg26 mice) and treatment with ART (emtricitabine; FTC) in female mice alters skeletal muscle homeostasis in an AhR-dependent manner to promote premature muscle aging phenotypes. Short-term FTC treatment increased serum KYN:tryptophan ratio and activated AhR signaling in skeletal muscle of Tg26 mice, although the study duration was not sufficient to induce significant FTC-related functional decline. FTC, alone or in combination with other ART (tenofovir alafenamide and tenofovir disproxil fumarate), activated AhR and induced senescence of female myoblasts in a manner comparable to KYN. Sequencing-based studies revealed targets and pathways related to the impacts of an HIV phenotype and ART in female skeletal muscle, including Gnas (encoding Gsα protein, critical for muscle glucose metabolism), inflammatory pathways, and lipid metabolism. Our studies suggest that the combined presence of HIV viral proteins and exposure to ART induced activation of AhR-mediated signaling in female muscle, as well as widespread changes across the skeletal muscle transcriptome and methylation landscape that may contribute to development of muscle dysfunction. This suggests AhR may represent a novel target for addressing persistent disparities in healthspan for PLWH.

抗逆转录病毒疗法(ART)降低了艾滋病毒相关死亡率,但艾滋病毒感染者(PLWH)长期使用抗逆转录病毒疗法与身体虚弱和健康状况不佳有关。驱动这种现象的机制尚不完全清楚,但临床和临床前研究表明,HIV和ART可能驱动犬尿氨酸(KYN)异常激活芳烃受体(AhR), KYN是一种内源性色氨酸代谢物。因此,我们研究了在雌性小鼠中,hiv样表型(Tg26小鼠)和ART(恩曲他滨;FTC)治疗是否以ahr依赖的方式改变骨骼肌稳态,从而促进肌肉过早衰老表型。短期FTC治疗增加了Tg26小鼠血清KYN:色氨酸比率,激活了骨骼肌AhR信号,尽管研究时间不足以诱导显著的FTC相关功能下降。FTC单独或与其他ART(替诺福韦阿拉那胺和富马酸替诺福韦双吡酯)联合,激活AhR并以与KYN相当的方式诱导女性成肌细胞衰老。基于测序的研究揭示了与HIV表型和ART在女性骨骼肌中的影响相关的靶点和途径,包括Gnas(编码Gsα蛋白,对肌肉葡萄糖代谢至关重要)、炎症途径和脂质代谢。我们的研究表明,HIV病毒蛋白的联合存在和ART暴露诱导了女性肌肉中ahr介导的信号的激活,以及骨骼肌转录组和甲基化的广泛变化,这可能有助于肌肉功能障碍的发展。这表明AhR可能是解决PLWH健康跨度持续差异的新目标。
{"title":"The antiretroviral drug emtricitabine increases kynurenine: tryptophan ratio, aryl hydrocarbon receptor activation, and cellular senescence in female mice.","authors":"Alok Tripathi, Shabiha Sultana, Sagar Vyavahare, Jie Chen, Arindam Paul, Huidong Shi, Wenbo Zhi, Rafal Pacholczyk, Bharati Mendhe, Apeksha Anand, Anthony Carrillo, Jaeshia Lindsay, Dima W Alhamad, Husam Bensreti, Christopher L Yearwood, Dylan Taylor, Colby Gross, Maribeth Johnson, Eric J Belin de Chantemele, Mark W Hamrick, Meghan E McGee-Lawrence","doi":"10.1016/j.biochi.2025.12.009","DOIUrl":"10.1016/j.biochi.2025.12.009","url":null,"abstract":"<p><p>HIV-associated mortality has been reduced by antiretroviral therapies (ART), but prolonged ART usage by people living with HIV (PLWH) is associated with frailty and poor healthspan. Mechanisms driving this phenomenon are not fully known, but clinical and preclinical studies suggest that HIV and ART may drive aberrant activation of the aryl hydrocarbon receptor (AhR) by kynurenine (KYN), an endogenous metabolite of tryptophan. Therefore, we investigated whether the combination of an HIV-like phenotype (Tg26 mice) and treatment with ART (emtricitabine; FTC) in female mice alters skeletal muscle homeostasis in an AhR-dependent manner to promote premature muscle aging phenotypes. Short-term FTC treatment increased serum KYN:tryptophan ratio and activated AhR signaling in skeletal muscle of Tg26 mice, although the study duration was not sufficient to induce significant FTC-related functional decline. FTC, alone or in combination with other ART (tenofovir alafenamide and tenofovir disproxil fumarate), activated AhR and induced senescence of female myoblasts in a manner comparable to KYN. Sequencing-based studies revealed targets and pathways related to the impacts of an HIV phenotype and ART in female skeletal muscle, including Gnas (encoding Gsα protein, critical for muscle glucose metabolism), inflammatory pathways, and lipid metabolism. Our studies suggest that the combined presence of HIV viral proteins and exposure to ART induced activation of AhR-mediated signaling in female muscle, as well as widespread changes across the skeletal muscle transcriptome and methylation landscape that may contribute to development of muscle dysfunction. This suggests AhR may represent a novel target for addressing persistent disparities in healthspan for PLWH.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145866702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The uptake of ingested vitamin B12 and its total body balance: a mathematical model suggests the optimal supplementation strategy. 摄取维生素B12及其全身平衡:一个数学模型建议最佳补充策略。
IF 3 Pub Date : 2025-12-06 DOI: 10.1016/j.biochi.2025.12.002
Sergey N Fedosov

Impaired or insufficient uptake of vitamin B12 causes neurological disorders, anemia, and various diffuse symptoms, all historically called pernicious anemia (PA). Maintenance of adequate B12 body store (B) is important, but the recommended doses and duration of peroral B12-supplementation are usually half-empirical. The current work suggests physiologically realistic algebraic equations to express the changes in B via the daily B12-uptake. The data from literature were used to estimate the relevant parameters of the equations. The modeled values of B showed that the daily ingestion of B12 = 3 × 2.0 μg maintains the steady state value of B = 1316/1858/2683 μg in healthy individuals with low/mean/high types of B12-uptake. The "classical" PA-patients have a highly decreased intrinsic factor (falling from 30 μg of B12-equivalents to below 0.2 μg), giving B = 47/81/123 μg for the low/mean/high B12-uptakes and the aforementioned doses. Alignment of B with the combined index of B12-status (cB12) in a heterogeneous cohort indicated that B > 1250 μg provides the safe B12-status for >84 % of the subjects. The risk of PA is associated with B < 400 μg. Repletion of a low body store from B = 400 μg to ≈1250 μg would require a prolonged supplementation of healthy individuals with B12-pills, if they receive 1 × 5 μg/day or 1 × 50 μg/day. These schemes are expected to raise B after the time intervals of (not possible)/2200/780 days or 2330/860/480 days, respectively. Only a pill with high B12 = 5000 μg/day would raise B to 1250 μg in 24/16/10 days.

维生素B12摄取受损或不足会导致神经系统疾病、贫血和各种弥漫性症状,这些在历史上都被称为恶性贫血(PA)。维持足够的B12体内储存(B)是很重要的,但建议的剂量和每次补充B12的持续时间通常是半经验的。目前的工作提出了生理上现实的代数方程来表达通过每日b12摄取的B的变化。利用文献资料估计方程的相关参数。B的模型值表明,在低/中/高B12摄取类型的健康个体中,每日摄入B12 = 3×2.0 μg可维持B = 1316/1858/2683 μg的稳态值。“经典”pa患者的内在因子(b12当量从30 μg降至0.2 μg以下)大幅降低,因此低/平均/高b12摄取和上述剂量的B = 47/81/123 μg。在一个异质队列中,B与b12状态综合指数(cB12)的比对表明,B >250 μg为84%的>受试者提供了安全的b12状态。当B < 400 μg时,患PA的风险增加。如果健康个体每天摄入1×5或1×50 μg/天的b12药片,那么从B = 400 μg到≈1250 μg的低体库的补充将需要长期补充b12药片。这些方案预计分别在(不可能)/2200/780天或2330/860/480天的时间间隔后提高B。仅服用高B12 = 5000 μg/d的药片,24/16/10天内B升高至1250 μg。
{"title":"The uptake of ingested vitamin B12 and its total body balance: a mathematical model suggests the optimal supplementation strategy.","authors":"Sergey N Fedosov","doi":"10.1016/j.biochi.2025.12.002","DOIUrl":"10.1016/j.biochi.2025.12.002","url":null,"abstract":"<p><p>Impaired or insufficient uptake of vitamin B<sub>12</sub> causes neurological disorders, anemia, and various diffuse symptoms, all historically called pernicious anemia (PA). Maintenance of adequate B<sub>12</sub> body store (B) is important, but the recommended doses and duration of peroral B<sub>12</sub>-supplementation are usually half-empirical. The current work suggests physiologically realistic algebraic equations to express the changes in B via the daily B<sub>12</sub>-uptake. The data from literature were used to estimate the relevant parameters of the equations. The modeled values of B showed that the daily ingestion of B<sub>12</sub> = 3 × 2.0 μg maintains the steady state value of B = 1316/1858/2683 μg in healthy individuals with low/mean/high types of B<sub>12</sub>-uptake. The \"classical\" PA-patients have a highly decreased intrinsic factor (falling from 30 μg of B<sub>12</sub>-equivalents to below 0.2 μg), giving B = 47/81/123 μg for the low/mean/high B<sub>12</sub>-uptakes and the aforementioned doses. Alignment of B with the combined index of B<sub>12</sub>-status (cB12) in a heterogeneous cohort indicated that B > 1250 μg provides the safe B<sub>12</sub>-status for >84 % of the subjects. The risk of PA is associated with B < 400 μg. Repletion of a low body store from B = 400 μg to ≈1250 μg would require a prolonged supplementation of healthy individuals with B<sub>12</sub>-pills, if they receive 1 × 5 μg/day or 1 × 50 μg/day. These schemes are expected to raise B after the time intervals of (not possible)/2200/780 days or 2330/860/480 days, respectively. Only a pill with high B<sub>12</sub> = 5000 μg/day would raise B to 1250 μg in 24/16/10 days.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145710466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of two longevity interventions, calorie restriction and rapamycin treatment, on the kynurenine-aryl hydrocarbon receptor pathway in aging skeletal muscle. 卡路里限制和雷帕霉素治疗两种长寿干预对衰老骨骼肌中犬尿氨酸-芳烃受体通路的影响
IF 3 Pub Date : 2025-11-20 DOI: 10.1016/j.biochi.2025.11.010
Mark W Hamrick, Sadanand Fulzele, Carlos M Isales, Meghan McGee-Lawrence

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is thought to play important roles in aging, oxidative stress, and cellular senescence. We have previously shown that the AhR agonist kynurenine (Kyn), a tryptophan metabolite that increases with age, can induce muscle atrophy in young mice. AhR overexpression can also lead to muscle atrophy and neuromuscular junction degradation. Here we utilized existing GEO data sets from skeletal muscles of aged mice to examine the impact of two longevity-related interventions, calorie restriction (CR) or treatment with the drug rapamycin (RM), on the expression of genes in the Kyn-AhR pathway. Data were examined in four skeletal muscles: soleus, gastrocnemius, tibialis anterior and triceps brachii. Results show that AhR expression increased with age in the triceps but was decreased with CR in the soleus and gastrocnemius. RM treatment did not significantly alter AhR expression in any of the four muscles of aged mice. Three enzymes that convert kynurenine to kynurenic acid in skeletal muscle, Kyat1, Kyat3 and Got2/Kyat4, are known to increase with endurance exercise and all three increased significantly with CR in aged skeletal muscle. In contrast, RM treatment did not increase Kyat1 expression in aged muscle and RM significantly decreased Kyat3 expression levels in muscles from aged mice. Together these data point to kynurenine aminotransferases as mediating some of the positive effects of CR on skeletal muscle with aging, and support prior research suggesting that CR and RM modulate different patterns of muscle-specific gene expression.

芳烃受体(AhR)是一种配体激活的转录因子,被认为在衰老、氧化应激和细胞衰老中起重要作用。我们之前已经证明,AhR激动剂犬尿氨酸(Kyn),一种色氨酸代谢物,随着年龄的增长而增加,可以诱导年轻小鼠的肌肉萎缩。AhR过表达也可导致肌肉萎缩和神经肌肉连接处退化。在这里,我们利用来自老年小鼠骨骼肌的现有GEO数据集来研究两种与长寿相关的干预措施,卡路里限制(CR)或药物雷帕霉素(RM)治疗对Kyn-AhR通路基因表达的影响。我们检查了四个骨骼肌的数据:比目鱼肌、腓肠肌、胫骨前肌和肱三头肌。结果表明,肱三头肌中AhR的表达随年龄增长而增加,而比目鱼肌和腓肠肌中CR的表达随年龄增长而降低。RM处理没有显著改变老年小鼠四种肌肉中AhR的表达。骨骼肌中有三种将犬尿氨酸转化为犬尿酸的酶Kyat1、Kyat3和Got2/Kyat4随着耐力运动而增加,这三种酶都随着老年骨骼肌CR的增加而显著增加。相反,RM没有增加老年小鼠肌肉中Kyat1的表达,但显著降低了老年小鼠肌肉中Kyat3的表达水平。综上所述,这些数据表明犬尿氨酸转氨酶介导了CR对骨骼肌衰老的一些积极作用,并支持了先前的研究,即CR和RM调节不同的肌肉特异性基因表达模式。
{"title":"Effects of two longevity interventions, calorie restriction and rapamycin treatment, on the kynurenine-aryl hydrocarbon receptor pathway in aging skeletal muscle.","authors":"Mark W Hamrick, Sadanand Fulzele, Carlos M Isales, Meghan McGee-Lawrence","doi":"10.1016/j.biochi.2025.11.010","DOIUrl":"10.1016/j.biochi.2025.11.010","url":null,"abstract":"<p><p>The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is thought to play important roles in aging, oxidative stress, and cellular senescence. We have previously shown that the AhR agonist kynurenine (Kyn), a tryptophan metabolite that increases with age, can induce muscle atrophy in young mice. AhR overexpression can also lead to muscle atrophy and neuromuscular junction degradation. Here we utilized existing GEO data sets from skeletal muscles of aged mice to examine the impact of two longevity-related interventions, calorie restriction (CR) or treatment with the drug rapamycin (RM), on the expression of genes in the Kyn-AhR pathway. Data were examined in four skeletal muscles: soleus, gastrocnemius, tibialis anterior and triceps brachii. Results show that AhR expression increased with age in the triceps but was decreased with CR in the soleus and gastrocnemius. RM treatment did not significantly alter AhR expression in any of the four muscles of aged mice. Three enzymes that convert kynurenine to kynurenic acid in skeletal muscle, Kyat1, Kyat3 and Got2/Kyat4, are known to increase with endurance exercise and all three increased significantly with CR in aged skeletal muscle. In contrast, RM treatment did not increase Kyat1 expression in aged muscle and RM significantly decreased Kyat3 expression levels in muscles from aged mice. Together these data point to kynurenine aminotransferases as mediating some of the positive effects of CR on skeletal muscle with aging, and support prior research suggesting that CR and RM modulate different patterns of muscle-specific gene expression.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145582822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Exercise-driven changes in tryptophan metabolism leading to healthy aging. 运动驱动的色氨酸代谢变化导致健康衰老。
IF 3 Pub Date : 2025-11-19 DOI: 10.1016/j.biochi.2025.11.004
Diana M Asante, Sagar Vyavahare, Mansi Shukla, Meghan E McGee-Lawrence, Carlos M Isales, Sadanand Fulzele

Tryptophan metabolism is a critical regulator of physiological and pathological processes, primarily through the kynurenine (KYN), serotonin and indole pathways. Dysregulation of indoleamine 2,3-dioxygenase 1 (IDO1) activity, serotonin and indole gut-microbial metabolism has been linked to a broad range of age-related chronic conditions, including cancer, cardiovascular disease, sarcopenia, and neurodegenerative disorders. Exercise emerges as a potent modulator of these pathways, redirecting tryptophan utilization to limit the accumulation of KYN metabolites while maintaining balanced indole and serotonin production. By regulating IDO1 activity and KYN flux, exercise alleviates inflammation, restores metabolic homeostasis, improved muscle integrity, neuroprotection, and overall systemic health. Mounting evidence supports the notion that lifestyle-based interventions targeting IDO1 and its downstream metabolites, particularly by physical activity, may offer a promising avenue for extending health span and mitigating the burden of chronic disease. This review synthesizes current advances in understanding the regulation of tryptophan metabolism (KYN, Serotonin and Indole) and highlights the unique capacity of exercise to remodel these pathways, underscoring their therapeutic potential in the context of healthy aging.

色氨酸代谢是生理和病理过程的关键调节因子,主要通过犬尿氨酸(KYN),血清素和吲哚途径。吲哚胺2,3-双加氧酶1 (IDO1)活性、血清素和吲哚肠道微生物代谢的失调与广泛的年龄相关的慢性疾病有关,包括癌症、心血管疾病、肌肉减少症和神经退行性疾病。运动是这些途径的有效调节剂,重定向色氨酸的利用,以限制KYN代谢物的积累,同时保持吲哚和血清素的平衡产生。通过调节IDO1活性和KYN通量,运动减轻炎症,恢复代谢稳态,改善肌肉完整性,神经保护和整体系统健康。越来越多的证据支持这样一种观点,即针对IDO1及其下游代谢物的基于生活方式的干预措施,特别是通过体育活动,可能为延长健康寿命和减轻慢性疾病负担提供了一条有希望的途径。这篇综述综合了目前对色氨酸代谢(KYN, 5 -羟色胺和吲哚)调节的理解进展,并强调了运动重塑这些途径的独特能力,强调了它们在健康衰老背景下的治疗潜力。
{"title":"Exercise-driven changes in tryptophan metabolism leading to healthy aging.","authors":"Diana M Asante, Sagar Vyavahare, Mansi Shukla, Meghan E McGee-Lawrence, Carlos M Isales, Sadanand Fulzele","doi":"10.1016/j.biochi.2025.11.004","DOIUrl":"10.1016/j.biochi.2025.11.004","url":null,"abstract":"<p><p>Tryptophan metabolism is a critical regulator of physiological and pathological processes, primarily through the kynurenine (KYN), serotonin and indole pathways. Dysregulation of indoleamine 2,3-dioxygenase 1 (IDO1) activity, serotonin and indole gut-microbial metabolism has been linked to a broad range of age-related chronic conditions, including cancer, cardiovascular disease, sarcopenia, and neurodegenerative disorders. Exercise emerges as a potent modulator of these pathways, redirecting tryptophan utilization to limit the accumulation of KYN metabolites while maintaining balanced indole and serotonin production. By regulating IDO1 activity and KYN flux, exercise alleviates inflammation, restores metabolic homeostasis, improved muscle integrity, neuroprotection, and overall systemic health. Mounting evidence supports the notion that lifestyle-based interventions targeting IDO1 and its downstream metabolites, particularly by physical activity, may offer a promising avenue for extending health span and mitigating the burden of chronic disease. This review synthesizes current advances in understanding the regulation of tryptophan metabolism (KYN, Serotonin and Indole) and highlights the unique capacity of exercise to remodel these pathways, underscoring their therapeutic potential in the context of healthy aging.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145575102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Highly specific aptamer trap for extremophilic RNA polymerases. 针对嗜极 RNA 聚合酶的高特异性适配体陷阱。
Pub Date : 2024-05-15 DOI: 10.1016/j.biochi.2024.05.014
Ivan Petushkov, Andrey Feklistov, Andrey Kulbachinskiy

During transcription initiation, the holoenzyme of bacterial RNA polymerase (RNAP) specifically recognizes promoters using a dedicated σ factor. During transcription elongation, the core enzyme of RNAP interacts with nucleic acids mainly nonspecifically, by stably locking the DNA template and RNA transcript inside the main cleft. Here, we present a synthetic DNA aptamer that is specifically recognized by both core and holoenzyme RNAPs from extremophilic bacteria of the Deinococcus-Thermus lineage. The aptamer binds RNAP with subnanomolar affinities, forming extremely stable complexes even at high ionic strength conditions, blocks RNAP interactions with the DNA template and inhibits RNAP activity during transcription elongation. We propose that the aptamer binds at a conserved site within the downstream DNA-binding cleft of RNAP and traps it in an inactive conformation. The aptamer can potentially be used for structural studies to reveal RNAP conformational states, affinity binding of RNAP and associated factors, and screening of transcriptional inhibitors.

在转录启动过程中,细菌 RNA 聚合酶(RNAP)的全酶利用专用的 σ 因子特异性地识别启动子。在转录延伸过程中,RNAP 的核心酶主要通过将 DNA 模板和 RNA 转录本稳定地锁定在主裂隙内与核酸进行非特异性相互作用。在这里,我们展示了一种合成的DNA适配体,它能被来自嗜极细菌(Deinococcus-Thermus lineage)的核心和全酶RNAP特异性识别。这种适配体能以亚纳摩尔级的亲和力与 RNAP 结合,即使在高离子强度条件下也能形成极其稳定的复合物,阻断 RNAP 与 DNA 模板的相互作用,并在转录延伸过程中抑制 RNAP 的活性。我们认为,该配合物与 RNAP 下游 DNA 结合裂隙中的一个保守位点结合,并使其处于非活性构象。这种适配体可用于结构研究以揭示 RNAP 的构象状态、RNAP 与相关因子的亲和结合以及转录抑制剂的筛选。
{"title":"Highly specific aptamer trap for extremophilic RNA polymerases.","authors":"Ivan Petushkov, Andrey Feklistov, Andrey Kulbachinskiy","doi":"10.1016/j.biochi.2024.05.014","DOIUrl":"https://doi.org/10.1016/j.biochi.2024.05.014","url":null,"abstract":"<p><p>During transcription initiation, the holoenzyme of bacterial RNA polymerase (RNAP) specifically recognizes promoters using a dedicated σ factor. During transcription elongation, the core enzyme of RNAP interacts with nucleic acids mainly nonspecifically, by stably locking the DNA template and RNA transcript inside the main cleft. Here, we present a synthetic DNA aptamer that is specifically recognized by both core and holoenzyme RNAPs from extremophilic bacteria of the Deinococcus-Thermus lineage. The aptamer binds RNAP with subnanomolar affinities, forming extremely stable complexes even at high ionic strength conditions, blocks RNAP interactions with the DNA template and inhibits RNAP activity during transcription elongation. We propose that the aptamer binds at a conserved site within the downstream DNA-binding cleft of RNAP and traps it in an inactive conformation. The aptamer can potentially be used for structural studies to reveal RNAP conformational states, affinity binding of RNAP and associated factors, and screening of transcriptional inhibitors.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140960867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inside front cover-EDB 内侧前盖EDB
Pub Date : 2023-10-17 DOI: 10.1016/S0300-9084(23)00260-2
{"title":"Inside front cover-EDB","authors":"","doi":"10.1016/S0300-9084(23)00260-2","DOIUrl":"https://doi.org/10.1016/S0300-9084(23)00260-2","url":null,"abstract":"","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":"214 ","pages":"Page IFC"},"PeriodicalIF":0.0,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49670825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Biochimie
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1