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Retraction Statement. 撤回声明。
Q3 CELL BIOLOGY Pub Date : 2023-12-31 DOI: 10.33594/000000676
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引用次数: 0
Retraction Statement. 撤回声明。
Q3 CELL BIOLOGY Pub Date : 2023-12-31 DOI: 10.33594/000000678
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引用次数: 0
Epistemology of the Origin of Cancer II: Fibroblasts Are the First Cells to Undergo Neoplastic Transformation. 癌症起源认识论 II:成纤维细胞是最先发生肿瘤性转化的细胞。
Q3 CELL BIOLOGY Pub Date : 2023-12-27 DOI: 10.33594/000000672
Björn L D M Brücher, Ijaz S Jamall

Background/aims: Many questions in cancer biology remain unanswered. Perhaps the most important issues remaining to be addressed focus on the molecular basis of carcinogenesis. Today's cancer focus lies on genetics and gene expression, which is unlikely to explain the true cause of most cancers or lead to a cure.

Methods: Earlier, we provided a plausible mechanism for this process, specifically, that most cancers develop in response to pathogenic stimuli that induce chronic inflammation, fibrosis, and remodeling of the cellular microenvironment. Collectively, these changes generate a precancerous niche (PCN) in which fibrosis and remodeling are ongoing secondary to persistent inflammation, followed by the deployment of a chronic stress escape strategy (CSES). If the CSES is unsuccessful, the cell undergoes a normal cell to cancer cell transformation (NCCT).

Results: Here, we highlight the critical role of fibroblasts as the first cells to undergo neoplastic transformation to a cancerous phenotype which is based on several critical findings. First, persistent disruption of homeostatic crosstalk increases lysyl oxidase activity and lysine oxidation which leads to increased collagen stiffness and decreased elasticity. If unresolved, chronic tissue stress will lead to an escape strategy that involves the recruitment of fibroblasts and fibrocytes from the bone marrow as well as cells undergoing an epithelial-mesenchymal transition (EMT). This yields a heterogeneous pool of cells that express both epithelial and mesenchymal markers and that will ultimately differentiate into cancer-associated fibroblasts (CAFs). Finally, CAFs undergo a mesenchymalepithelial transition (MET) and express epithelial markers that facilitate their integration into the target tissue.

Conclusion: Here, we review the published findings that led us to this conclusion which is the most plausible answer to this critical question.

背景/目的:癌症生物学的许多问题仍未得到解答。有待解决的最重要问题可能是致癌的分子基础。当今癌症研究的重点在于遗传学和基因表达,这不可能解释大多数癌症的真正原因,也不可能导致治愈:方法:早些时候,我们为这一过程提供了一个貌似合理的机制,具体来说,大多数癌症都是在致病刺激的作用下发生的,这些刺激会诱发慢性炎症、纤维化和细胞微环境的重塑。这些变化共同产生了一个癌前生态位(PCN),在这个生态位中,纤维化和重塑继发于持续的炎症,随后是慢性应激逃逸策略(CSES)的部署。如果CSES不成功,细胞就会经历正常细胞向癌细胞的转化(NCCT):结果:在此,我们强调了成纤维细胞的关键作用,它们是向癌表型发生肿瘤性转化的第一批细胞。首先,同种异化作用的持续破坏会增加赖氨酰氧化酶的活性和赖氨酸的氧化,从而导致胶原蛋白硬度增加和弹性降低。如果不加以解决,慢性组织压力将导致一种逃逸策略,即从骨髓中招募成纤维细胞和纤维细胞,以及进行上皮-间质转化(EMT)的细胞。这就产生了一个同时表达上皮和间质标记的异质细胞池,这些细胞最终会分化成癌症相关成纤维细胞(CAFs)。最后,CAFs 会发生间质上皮转化(MET),并表达上皮标记,从而促进其与靶组织的整合:在此,我们回顾了导致我们得出这一结论的已发表的研究结果,这是对这一关键问题最合理的回答。
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引用次数: 0
Mechanisms of Senescence in Cancer: Positive and Negative Aspects of Cancer Cells Senescence 癌症中的衰老机制:癌细胞衰老的积极和消极方面
Q3 CELL BIOLOGY Pub Date : 2023-12-06 DOI: 10.33594/000000671
Cell senescence was considered an attribute of normal dividing cells, which distinguishing them from cancer cells that do not have a division limit. However, recent studies show that senescence could also occur in cancer cells. Cancer cell senescence could occur as a result of chemotherapy, radiation, inhibition of telomerase activity, induction of DNA damage, changes in the tumor microenvironment, regulation of senescence-related proteins, oxidative stress, inflammation, or epigenetic dysregulation. It seems that the induction of senescence in cancer cells could significantly affect the inhibition of tumor progression, but in some types of cancer, it can affect their invasive character. Furthermore, considering the therapeutic implications of this process, it is essential to consider the positive and negative aspects of cancer cell senescence. It is crucial to understand the molecular mechanisms that induce senescence under specific conditions, considering the potential hazards. In the future, the senescence of cancer cells may contribute to using this property in modern cancer treatment strategies.
细胞衰老被认为是正常分裂细胞的一种特征,这将它们与没有分裂限制的癌细胞区分开来。然而,最近的研究表明,衰老也可能发生在癌细胞中。化疗、放疗、端粒酶活性的抑制、DNA损伤的诱导、肿瘤微环境的改变、衰老相关蛋白的调节、氧化应激、炎症或表观遗传失调都可能导致癌细胞衰老。似乎诱导癌细胞衰老可以显著影响肿瘤进展的抑制,但在某些类型的癌症中,它可以影响其侵袭性。此外,考虑到这一过程的治疗意义,必须考虑癌细胞衰老的积极和消极方面。考虑到潜在的危害,了解在特定条件下诱导衰老的分子机制是至关重要的。在未来,癌细胞的衰老可能有助于在现代癌症治疗策略中使用这一特性。
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引用次数: 0
Do the Effects of Krebs Cycle Intermediates on Oxygen-Dependent Processes in Hypoxia Mediated by the Nitric Oxide System Have Reciprocal or Competitive Relationships? 由一氧化氮系统介导的缺氧中克雷布斯循环中间体对氧依赖过程的影响是否具有互惠或竞争关系?
Q3 CELL BIOLOGY Pub Date : 2023-11-15 DOI: 10.33594/000000669
Natalia Kurhaluk, Oleksandr Lukash, Halina Tkaczenko

Background/aims: Currently, it is proven that the cellular metabolism of nitric oxide is necessary to maintain optimal health and adaptation of the organism to the impact of various environmental factors. The aim of this work was to reveal the biological role of nitric oxide, its metabolic changes, and its mechanism of action in tissues under hypoxia, as well as the possibility of tissue metabolism correction through NO-dependent systems under the influence of Krebs cycle intermediates.

Methods: A systematic assessment of the effect of succinate (SC, 50 mg/kg b.w.) and α-ketoglutarate (KGL, 50 mg/kg b.w.) in the regulation of oxygendependent processes in rats (mitochondrial oxidative phosphorylation, microsomal oxidation, intensity of lipid peroxidation processes, and the state of the antioxidant defense system) depending on functional changes in nitric oxide production during hypoxia was evaluated. The state of the nitric oxide system was estimated spectrophotometrically by determination of the concentration of its stable nitrite anion metabolite (NO2 -). The levels of catecholamines were estimated from the content of epinephrine and norepinephrine using the differentially fluorescent method. The activity of cytochrome P450-dependent aminopyrine-N-demethylase was determined with the Nash reagent.

Results: Tissue hypoxia and metabolic disorders caused by this condition through changes in the content of catecholamines (epinephrine, norepinephrine, dopamine, DOPA) as well as the cholinesterase-related system (acetylcholine content and acetylcholinesterase activity) were the studied experimental parameters under acute hypoxia (AH, 7% O2 in N2, 30 min). The activation of lipid peroxidation and oxidatively modified proteins and an increase in the epinephrine content in AH are associated with an increased role of SC and a decrease in KGL as substrates of oxidation in mitochondria. A more pronounced effect of exogenous KGL, compared to SC, on the content of nitrite anion as a stable metabolite of nitric oxide in the liver under acute hypoxia against the background of a decrease in the intensity of lipid peroxidation processes was revealed. The activation of SC-dependent mitochondrial oxidative processes caused by AH was found to decrease in animals after an intermittent hypoxia training (IHT) course. IHT (7% O2 in N2, 15-min, 5 times daily, 14 days) prevented the activation of oxidative stress in tissues and blood after the AH impact and increased the efficiency of energy-related reactions in the functioning of hepatic mitochondria through increased oxidation of KGL.

Conclusion: The studied effects of adaptation are mediated by an increase in the role of NO-dependent mechanisms, as assessed by changes in the pool of nitrates, nitrites, carbamides, and total polyamines.

背景/目的:目前已经证明,一氧化氮的细胞代谢是维持机体最佳健康和适应各种环境因素影响所必需的。本研究旨在揭示缺氧条件下一氧化氮的生物学作用、代谢变化及其在组织中的作用机制,以及在克雷布斯循环中间体的影响下,一氧化氮依赖系统对组织代谢进行校正的可能性。方法:系统评估琥珀酸盐(SC, 50 mg/kg b.w.)和α-酮戊二酸盐(KGL, 50 mg/kg b.w.)对缺氧时一氧化氮生成的功能变化对大鼠氧依赖过程(线粒体氧化磷酸化、微粒体氧化、脂质过氧化过程强度和抗氧化防御系统状态)的调节作用。用分光光度法测定其稳定的亚硝酸盐阴离子代谢物(NO2 -)的浓度来估计一氧化氮体系的状态。儿茶酚胺的水平是用差异荧光法从肾上腺素和去甲肾上腺素的含量来估计的。采用Nash试剂测定细胞色素p450依赖性氨基吡啶- n -去甲基化酶的活性。结果:研究急性缺氧(AH, 7% O2 in N2, 30min)下组织缺氧及由此引起的儿茶酚胺(肾上腺素、去甲肾上腺素、多巴胺、多巴胺)含量变化及胆碱酯酶相关系统(乙酰胆碱含量和乙酰胆碱酯酶活性)代谢紊乱的实验参数。AH中脂质过氧化和氧化修饰蛋白的激活以及肾上腺素含量的增加与SC作为线粒体氧化底物的作用增加和KGL的减少有关。与SC相比,外源性KGL对急性缺氧下肝脏中一氧化氮的稳定代谢物亚硝酸盐阴离子含量的影响更为明显,其背景是脂质过氧化过程的强度降低。间歇性缺氧训练(IHT)后,发现AH引起的sc依赖性线粒体氧化过程的激活减少。IHT (7% O2在N2中,15分钟,每天5次,14天)阻止AH冲击后组织和血液中氧化应激的激活,并通过增加KGL的氧化提高肝线粒体功能中能量相关反应的效率。结论:通过硝酸盐、亚硝酸盐、氨酰胺和总多胺的变化来评估,所研究的适应效应是由no依赖机制的作用增加介导的。
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引用次数: 0
Evaluation of Stem Cell Laden Collagen + Polycaprolactone + Multi-Walled Carbon Nano-Tubes Nano-Neural Scaffold with and Without Insulin Like Growth Factor-I For Sciatic Nerve Regeneration Post Crush Injury in Wistar Rats. 干细胞负载胶原+聚己内酯+多壁碳纳米管纳米神经支架在Wistar大鼠坐骨神经挤压损伤后再生中的应用
Q3 CELL BIOLOGY Pub Date : 2023-11-15 DOI: 10.33594/000000670
Mamta Mishra, Swapan Kumar Maiti, Kalaiselvan Elangovan, Shivaraju Shivaramu, Karam Pal Singh, Amitha Banu S, Merlin Mamachan, Manish Arya, Divya Mishra, Jurgen Hescheler

Background/aims: All body functions are activated, synchronized and controlled by a substantial, complex network, the nervous system. Upon injury, pathophysiology of the nerve injury proceeds through different paths. The axon may undergo a degenerative retraction from the site of injury for a short distance unless the injury is near to the cell body, in which case it continues to the soma and undergoes retrograde neuronal degeneration. Otherwise, the distal section suffers from Wallerian degeneration, which is marked by axonal swelling, spheroids, and cytoskeleton degeneration. The objective of the study was to evaluate the potential of mesenchymal stem cell laden neural scaffold and insulin-like growth factor I (IGF-I) in nerve regeneration following sciatic nerve injury in a rat model.

Methods: The animals were anaesthetized and a cranio-lateral incision over left thigh was made. Sciatic nerve was exposed and crush injury was introduced for 90 seconds using haemostat at second locking position. The muscle and skin were sutured in routine fashion and thus the rat model of sciatic crush injury was prepared. The animal models were equally distributed into 5 different groups namely A, B, C, D and E and treated with phosphate buffer saline (PBS), carbon nanotubes based neural scaffold only, scaffold with IGF-I, stem cell laden scaffold and stem cell laden scaffold with IGF-I respectively. In vitro scaffold testing was performed. The nerve regeneration was assessed based on physico-neuronal, biochemical, histopathological examination, and relative expression of NRP-1, NRP-2 and GAP-43 and scanning electron microscopy.

Results: Sciatic nerve injury model with crush injury produced for 90 seconds was standardized and successfully used in this study. All the biochemical parameters were in normal range in all the groups indicating no scaffold related changes. Physico-neuronal, histopathological, relative gene expression and scanning electron microscopy observations revealed appreciable nerve regeneration in groups E and D, followed by C and B. Restricted to no regeneration was observed in group A.

Conclusion: Carbon nanotubes based scaffold provided electro-conductivity for proper neuronal regeneration while rat bone marrow-derived mesenchymal stem cells were found to induce axonal sprouting, cellular transformation; whereas IGF-I induced stem cell differentiation, myelin synthesis, angiogenesis and muscle differentiation.

背景/目的:所有的身体功能都是由一个庞大而复杂的网络——神经系统——激活、同步和控制的。损伤后,神经损伤的病理生理经过不同的途径。轴突可能从损伤部位退行性缩回一小段距离,除非损伤靠近细胞体,在这种情况下,它继续到体细胞并经历逆行神经元变性。否则,远端部分出现沃勒氏变性,其特征是轴突肿胀、球状体和细胞骨架变性。本研究的目的是评估间充质干细胞负载神经支架和胰岛素样生长因子I (IGF-I)在大鼠坐骨神经损伤后神经再生中的潜力。方法:麻醉动物,在左大腿上开颅外侧切口。暴露坐骨神经,在第二锁定位置使用止血剂进行挤压损伤90秒。采用常规方法缝合肌肉和皮肤,制备大鼠坐骨挤压损伤模型。将动物模型平均分为A、B、C、D、E 5组,分别采用磷酸缓冲盐水(PBS)、碳纳米管神经支架、IGF-I支架、干细胞负载支架和IGF-I干细胞负载支架处理。进行体外支架试验。通过物理-神经元、生化、组织病理学检查,以及NRP-1、NRP-2、GAP-43的相对表达和扫描电镜评估神经再生情况。结果:90秒挤压伤坐骨神经损伤模型标准化并成功应用于本研究。各组生化指标均在正常范围内,未见支架相关变化。物理-神经元、组织病理学、相关基因表达和扫描电镜观察显示,E组和D组有明显的神经再生,其次是C组和b组,a组没有再生。结论:碳纳米管支架为神经再生提供了电导率,而大鼠骨髓源间充质干细胞可诱导轴突萌发、细胞转化;而igf - 1诱导干细胞分化、髓磷脂合成、血管生成和肌肉分化。
{"title":"Evaluation of Stem Cell Laden Collagen + Polycaprolactone + Multi-Walled Carbon Nano-Tubes Nano-Neural Scaffold with and Without Insulin Like Growth Factor-I For Sciatic Nerve Regeneration Post Crush Injury in Wistar Rats.","authors":"Mamta Mishra, Swapan Kumar Maiti, Kalaiselvan Elangovan, Shivaraju Shivaramu, Karam Pal Singh, Amitha Banu S, Merlin Mamachan, Manish Arya, Divya Mishra, Jurgen Hescheler","doi":"10.33594/000000670","DOIUrl":"10.33594/000000670","url":null,"abstract":"<p><strong>Background/aims: </strong>All body functions are activated, synchronized and controlled by a substantial, complex network, the nervous system. Upon injury, pathophysiology of the nerve injury proceeds through different paths. The axon may undergo a degenerative retraction from the site of injury for a short distance unless the injury is near to the cell body, in which case it continues to the soma and undergoes retrograde neuronal degeneration. Otherwise, the distal section suffers from Wallerian degeneration, which is marked by axonal swelling, spheroids, and cytoskeleton degeneration. The objective of the study was to evaluate the potential of mesenchymal stem cell laden neural scaffold and insulin-like growth factor I (IGF-I) in nerve regeneration following sciatic nerve injury in a rat model.</p><p><strong>Methods: </strong>The animals were anaesthetized and a cranio-lateral incision over left thigh was made. Sciatic nerve was exposed and crush injury was introduced for 90 seconds using haemostat at second locking position. The muscle and skin were sutured in routine fashion and thus the rat model of sciatic crush injury was prepared. The animal models were equally distributed into 5 different groups namely A, B, C, D and E and treated with phosphate buffer saline (PBS), carbon nanotubes based neural scaffold only, scaffold with IGF-I, stem cell laden scaffold and stem cell laden scaffold with IGF-I respectively. In vitro scaffold testing was performed. The nerve regeneration was assessed based on physico-neuronal, biochemical, histopathological examination, and relative expression of NRP-1, NRP-2 and GAP-43 and scanning electron microscopy.</p><p><strong>Results: </strong>Sciatic nerve injury model with crush injury produced for 90 seconds was standardized and successfully used in this study. All the biochemical parameters were in normal range in all the groups indicating no scaffold related changes. Physico-neuronal, histopathological, relative gene expression and scanning electron microscopy observations revealed appreciable nerve regeneration in groups E and D, followed by C and B. Restricted to no regeneration was observed in group A.</p><p><strong>Conclusion: </strong>Carbon nanotubes based scaffold provided electro-conductivity for proper neuronal regeneration while rat bone marrow-derived mesenchymal stem cells were found to induce axonal sprouting, cellular transformation; whereas IGF-I induced stem cell differentiation, myelin synthesis, angiogenesis and muscle differentiation.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"57 6","pages":"452-477"},"PeriodicalIF":0.0,"publicationDate":"2023-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136396594","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
Docosahexaenoic Acid (DHA) Reduces LPS-Induced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/Syk Signaling-Dependent Phagocytosis in Microglia. 二十二碳六烯酸(DHA)通过ATF3转录因子减少脂多糖诱导的炎症反应并刺激小胶质细胞Src/Syk信号依赖性吞噬。
Q3 CELL BIOLOGY Pub Date : 2023-11-13 DOI: 10.33594/000000668
Katarzyna Wieczorek-Szukala, Monika Markiewicz, Anna Walczewska, Emilia Zgorzynska

Background/aims: Microglial cells play a crucial role in the development of neuroinflammation in response to harmful stimuli, such as infection, ischemia or injury. Their chronic activation, however, is associated with a progression of neurodegenerative diseases. Therefore, looking for potential factors limiting microglial activation, the effect of docosahexaenoic acid (DHA) on the inflammatory response and TREM2-dependent phagocytic activity in microglia was investigated.

Methods: In LPS-induced primary microglia preincubated with DHA, or without preincubation the expression of ATF3 and TREM2 genes and TREM2, Syk, Akt proteins were determined by RT-PCR and WB, respectively. Cell viability was assayed by MTT and cytokine and chemokine expression was determined by the Proteome Profiler assay. Moreover, the phagocytic activity of microglia was assayed using immunofluorescence.

Results: We found that DHA significantly increased the expression of ATF3 , and decreased the levels of CINC-1, CINC-2αβ, CINC-3 chemokines, IL-1α and IL-1β cytokines, and ICAM-1 adhesion protein. Additionally, preincubation of microglia with DHA resulted in increased Src/Syk kinases activation associated with increased phagocytic microglia activity.

Conclusion: These findings indicate that DHA efficiently inhibits ATF3-dependent release of proinflammatory mediators and enhances phagocytic activity of microglia. The study provides a new mechanism of DHA action in reactive microglia, which may help limit neuronal damage caused by the pro-inflammatory milieu in the brain.

背景/目的:小胶质细胞在对有害刺激(如感染、缺血或损伤)的神经炎症反应的发展中起着至关重要的作用。然而,它们的慢性激活与神经退行性疾病的进展有关。因此,为了寻找限制小胶质细胞激活的潜在因素,我们研究了二十二碳六烯酸(DHA)对小胶质细胞炎症反应和trem2依赖性吞噬活性的影响。方法:采用RT-PCR和WB分别检测脂多糖诱导的原代小胶质细胞中ATF3、TREM2基因和TREM2、Syk、Akt蛋白的表达。MTT法检测细胞活力,Proteome Profiler法检测细胞因子和趋化因子表达。免疫荧光法检测小胶质细胞的吞噬活性。结果:我们发现DHA显著提高了ATF3的表达,降低了cnc -1、cnc -2αβ、cnc -3趋化因子、IL-1α和IL-1β细胞因子以及ICAM-1粘附蛋白的水平。此外,用DHA预孵育小胶质细胞导致Src/Syk激酶活化增加,这与吞噬小胶质细胞活性增加有关。结论:DHA能有效抑制atf3依赖性促炎介质的释放,增强小胶质细胞的吞噬活性。该研究为DHA在反应性小胶质细胞中的作用提供了一种新的机制,这可能有助于限制大脑中促炎环境引起的神经元损伤。
{"title":"Docosahexaenoic Acid (DHA) Reduces LPS-Induced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/Syk Signaling-Dependent Phagocytosis in Microglia.","authors":"Katarzyna Wieczorek-Szukala, Monika Markiewicz, Anna Walczewska, Emilia Zgorzynska","doi":"10.33594/000000668","DOIUrl":"10.33594/000000668","url":null,"abstract":"<p><strong>Background/aims: </strong>Microglial cells play a crucial role in the development of neuroinflammation in response to harmful stimuli, such as infection, ischemia or injury. Their chronic activation, however, is associated with a progression of neurodegenerative diseases. Therefore, looking for potential factors limiting microglial activation, the effect of docosahexaenoic acid (DHA) on the inflammatory response and TREM2-dependent phagocytic activity in microglia was investigated.</p><p><strong>Methods: </strong>In LPS-induced primary microglia preincubated with DHA, or without preincubation the expression of ATF3 and TREM2 genes and TREM2, Syk, Akt proteins were determined by RT-PCR and WB, respectively. Cell viability was assayed by MTT and cytokine and chemokine expression was determined by the Proteome Profiler assay. Moreover, the phagocytic activity of microglia was assayed using immunofluorescence.</p><p><strong>Results: </strong>We found that DHA significantly increased the expression of ATF3 , and decreased the levels of CINC-1, CINC-2αβ, CINC-3 chemokines, IL-1α and IL-1β cytokines, and ICAM-1 adhesion protein. Additionally, preincubation of microglia with DHA resulted in increased Src/Syk kinases activation associated with increased phagocytic microglia activity.</p><p><strong>Conclusion: </strong>These findings indicate that DHA efficiently inhibits ATF3-dependent release of proinflammatory mediators and enhances phagocytic activity of microglia. The study provides a new mechanism of DHA action in reactive microglia, which may help limit neuronal damage caused by the pro-inflammatory milieu in the brain.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"57 6","pages":"411-425"},"PeriodicalIF":0.0,"publicationDate":"2023-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92152958","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
Erratum. 勘误表。
Q3 CELL BIOLOGY Pub Date : 2023-10-31 DOI: 10.33594/000000666
{"title":"Erratum.","authors":"","doi":"10.33594/000000666","DOIUrl":"10.33594/000000666","url":null,"abstract":"","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"57 5","pages":"409"},"PeriodicalIF":0.0,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71410921","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
Retraction Statement. 撤回声明。
Q3 CELL BIOLOGY Pub Date : 2023-10-31 DOI: 10.33594/000000667
{"title":"Retraction Statement.","authors":"","doi":"10.33594/000000667","DOIUrl":"10.33594/000000667","url":null,"abstract":"","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"57 5","pages":"410"},"PeriodicalIF":0.0,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71410922","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
Emerging Roles of SPT5 in Transcription. SPT5在转录中的新作用
Q3 CELL BIOLOGY Pub Date : 2023-10-23 DOI: 10.33594/000000665
Vivek Pandey, Shirani Punniyamoorthy, Yuba Raj Pokharel

Suppressor of Ty homolog-5 (SPT5) discovered in the yeast mutant screens as a suppressor of mutation caused by the insertion of the Transposons of yeast (Ty) element along with SPT4, with which it forms a holoenzyme complex known as DRB sensitivity-inducing factor (DSIF) and plays an essential role in the regulation of transcription. SPT5 is a highly conserved protein across all three domains of life and performs critical functions in transcription, starting from promoter-proximal pausing to termination. We also highlight the emerging role of SPT5 in other non-canonical functions, such as the regulation of post-translational modifications (PTM) and the transcriptional regulation of non-coding genes. Also, in brief, we highlight the clinical implications of SPT5 dysregulation.

在酵母突变体中发现的Ty同源物抑制剂-5(SPT5)筛选为酵母转座子(Ty)元件与SPT4一起插入引起的突变的抑制剂,与之形成称为DRB敏感性诱导因子(DSIF)的全酶复合物,并在转录调控中发挥重要作用。SPT5是一种高度保守的蛋白质,横跨生命的所有三个结构域,在转录中发挥关键功能,从启动子近端暂停到终止。我们还强调了SPT5在其他非经典功能中的新作用,如翻译后修饰(PTM)的调节和非编码基因的转录调节。此外,简而言之,我们强调了SPT5失调的临床意义。
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引用次数: 0
期刊
Cellular Physiology and Biochemistry
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