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Correction: The chaperonin CCT interacts with and mediates the correct folding and activity of three subunits of translation initiation factor eIF3: b, i and h. 更正:伴侣素 CCT 与翻译起始因子 eIF3 的三个亚基(b、i 和 h)相互作用,并介导其正确折叠和活性。
IF 4.1 3区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-06-19 DOI: 10.1042/BJ20130979_COR
Anne Roobol, Jo Roobol, Martin J Carden, Matthew E Smith, John W B Hershey, Amandine Bastide, John R P Knight, Anne E Willis, C Mark Smales
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引用次数: 0
Mechanisms and pathologies of human mitochondrial DNA replication and deletion formation. 人类线粒体 DNA 复制和缺失形成的机制和病理。
IF 4.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-05 DOI: 10.1042/BCJ20230262
Tiago M Bernardino Gomes, Amy E Vincent, Katja E Menger, James B Stewart, Thomas J Nicholls

Human mitochondria possess a multi-copy circular genome, mitochondrial DNA (mtDNA), that is essential for cellular energy metabolism. The number of copies of mtDNA per cell, and their integrity, are maintained by nuclear-encoded mtDNA replication and repair machineries. Aberrant mtDNA replication and mtDNA breakage are believed to cause deletions within mtDNA. The genomic location and breakpoint sequences of these deletions show similar patterns across various inherited and acquired diseases, and are also observed during normal ageing, suggesting a common mechanism of deletion formation. However, an ongoing debate over the mechanism by which mtDNA replicates has made it difficult to develop clear and testable models for how mtDNA rearrangements arise and propagate at a molecular and cellular level. These deletions may impair energy metabolism if present in a high proportion of the mtDNA copies within the cell, and can be seen in primary mitochondrial diseases, either in sporadic cases or caused by autosomal variants in nuclear-encoded mtDNA maintenance genes. These mitochondrial diseases have diverse genetic causes and multiple modes of inheritance, and show notoriously broad clinical heterogeneity with complex tissue specificities, which further makes establishing genotype-phenotype relationships challenging. In this review, we aim to cover our current understanding of how the human mitochondrial genome is replicated, the mechanisms by which mtDNA replication and repair can lead to mtDNA instability in the form of large-scale rearrangements, how rearranged mtDNAs subsequently accumulate within cells, and the pathological consequences when this occurs.

人类线粒体拥有多拷贝环状基因组--线粒体 DNA(mtDNA),它对细胞能量代谢至关重要。每个细胞的 mtDNA 副本数量及其完整性由核编码的 mtDNA 复制和修复机制维持。异常的 mtDNA 复制和 mtDNA 断裂被认为会导致 mtDNA 的缺失。这些缺失的基因组位置和断点序列在各种遗传性和获得性疾病中显示出相似的模式,在正常衰老过程中也能观察到,这表明缺失的形成有一个共同的机制。然而,由于对 mtDNA 复制机制的争论不休,因此很难建立清晰、可检验的模型来说明 mtDNA 重排是如何在分子和细胞水平上产生和传播的。如果细胞内的 mtDNA 副本比例过高,这些缺失就会损害能量代谢,原发性线粒体疾病就会出现这种情况,这些疾病可能是偶发病例,也可能是由核编码的 mtDNA 维护基因中的常染色体变异引起的。这些线粒体疾病具有不同的遗传原因和多种遗传方式,临床表现出广泛的异质性和复杂的组织特异性,这使得建立基因型与表型之间的关系变得更具挑战性。在这篇综述中,我们旨在介绍我们目前对人类线粒体基因组如何复制、mtDNA 复制和修复导致大规模重排形式的 mtDNA 不稳定性的机制、重排的 mtDNA 随后如何在细胞内积累以及发生这种情况时的病理后果的理解。
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引用次数: 0
The monodomain Kunitz protein EgKU-7 from the dog tapeworm Echinococcus granulosus is a high-affinity trypsin inhibitor with two interaction sites. 来自犬带绦虫棘球蚴的单链库尼茨蛋白 EgKU-7 是一种高亲和力胰蛋白酶抑制剂,具有两个相互作用位点。
IF 4.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-05 DOI: 10.1042/BCJ20230514
Martín Fló, Leonardo Pellizza, Rosario Durán, Beatriz Alvarez, Cecilia Fernández

Typical Kunitz proteins (I2 family of the MEROPS database, Kunitz-A family) are metazoan competitive inhibitors of serine peptidases that form tight complexes of 1:1 stoichiometry, mimicking substrates. The cestode Echinococcus granulosus, the dog tapeworm causing cystic echinococcosis in humans and livestock, encodes an expanded family of monodomain Kunitz proteins, some of which are secreted to the dog host interface. The Kunitz protein EgKU-7 contains, in addition to the Kunitz domain with the anti-peptidase loop comprising a critical arginine, a C-terminal extension of ∼20 amino acids. Kinetic, electrophoretic, and mass spectrometry studies using EgKU-7, a C-terminally truncated variant, and a mutant in which the critical arginine was substituted by alanine, show that EgKU-7 is a tight inhibitor of bovine and canine trypsins with the unusual property of possessing two instead of one site of interaction with the peptidases. One site resides in the anti-peptidase loop and is partially hydrolyzed by bovine but not canine trypsins, suggesting specificity for the target enzymes. The other site is located in the C-terminal extension. This extension can be hydrolyzed in a particular arginine by cationic bovine and canine trypsins but not by anionic canine trypsin. This is the first time to our knowledge that a monodomain Kunitz-A protein is reported to have two interaction sites with its target. Considering that putative orthologs of EgKU-7 are present in other cestodes, our finding unveils a novel piece in the repertoire of peptidase-inhibitor interactions and adds new notes to the evolutionary host-parasite concerto.

典型的库尼茨蛋白(MEROPS 数据库中的 I2 家族,库尼茨-A 家族)是丝氨酸肽酶的元虫竞争性抑制剂,能模仿底物形成 1:1 的紧密复合物。在人类和家畜中引起囊性棘球蚴病的犬带绦虫--棘球蚴粒球绦虫--编码一个扩大的单域 Kunitz 蛋白家族,其中一些蛋白被分泌到犬宿主界面。库尼茨蛋白 EgKU-7 除了包含由关键精氨酸组成的抗肽酶环的库尼茨结构域外,还含有一个约 20 个氨基酸的 C 端延伸。使用 EgKU-7、一个 C 端截短的变体和一个关键精氨酸被丙氨酸取代的突变体进行的动力学、电泳和质谱研究表明,EgKU-7 是牛和犬胰蛋白酶的紧密抑制剂,它具有与肽酶相互作用的两个而不是一个位点的不寻常特性。其中一个位点位于抗肽酶环,可被牛胰蛋白酶部分水解,但不能被犬胰蛋白酶水解,这表明它对目标酶具有特异性。另一个位点位于 C 端延伸部分。阳离子牛胰蛋白酶和犬胰蛋白酶能水解该延伸部分的特定精氨酸,但阴离子犬胰蛋白酶却不能。据我们所知,这是首次报道单结构域的 Kunitz-A 蛋白与其靶标有两个相互作用位点。考虑到 EgKU-7 的推测直向同源物存在于其他绦虫中,我们的发现揭开了抑肽酶相互作用的新篇章,为宿主-寄生虫进化协奏曲增添了新的音符。
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引用次数: 0
Efficient overexpression and purification of severe acute respiratory syndrome coronavirus 2 nucleocapsid proteins in Escherichia coli. 在大肠杆菌中高效过表达和纯化 SARS-CoV-2 核壳蛋白。
IF 4.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-05 DOI: 10.1042/BCJ20240019
Emma L Brudenell, Manoj B Pohare, Domen Zafred, Janine Phipps, Hailey R Hornsby, John F Darby, Junxiao Dai, Ellen Liggett, Kathleen M Cain, Perdita E Barran, Thushan I de Silva, Jon R Sayers

The fundamental biology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleocapsid protein (Ncap), its use in diagnostic assays and its potential application as a vaccine component have received considerable attention since the outbreak of the Covid19 pandemic in late 2019. Here we report the scalable expression and purification of soluble, immunologically active, SARS-CoV-2 Ncap in Escherichia coli. Codon-optimised synthetic genes encoding the original Ncap sequence and four common variants with an N-terminal 6His affinity tag (sequence MHHHHHHG) were cloned into an inducible expression vector carrying a regulated bacteriophage T5 synthetic promoter controlled by lac operator binding sites. The constructs were used to express Ncap proteins and protocols developed which allow efficient production of purified Ncap with yields of over 200 mg per litre of culture media. These proteins were deployed in ELISA assays to allow comparison of their responses to human sera. Our results suggest that there was no detectable difference between the 6His-tagged and untagged original Ncap proteins but there may be a slight loss of sensitivity of sera to other Ncap isolates.

自 2019 年底 Covid19 大流行爆发以来,严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)核噬菌体蛋白(Ncap)的基本生物学特性、其在诊断测试中的应用以及作为疫苗成分的潜在应用受到了广泛关注。 在此,我们报告了在大肠杆菌中可溶性表达和纯化具有免疫活性的 SARS-CoV-2 Ncap 的情况。编码原始 Ncap 序列和四种带有 N 端 6His 亲和标签(序列 MHHHHHHG)的常见变体的密码子优化合成基因被克隆到一个可诱导表达载体中,该载体携带一个由 lac 操作者结合位点控制的受调控噬菌体 T5 合成启动子。 这些构建体用于表达 Ncap 蛋白,所开发的方案可高效生产纯化的 Ncap,每升培养基的产量超过 200 毫克。这些蛋白质被用于酶联免疫吸附试验,以比较它们对人类血清的反应。 我们的结果表明,6His 标记和未标记的原始 Ncap 蛋白之间没有可检测到的差异,但血清对其他 Ncap 分离物的敏感性可能会略有下降。
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引用次数: 0
Validation of GCN5L1/BLOC1S1/BLOS1 antibodies using knockout cells and tissue. 利用基因敲除细胞和组织验证 GCN5L1/BLOC1S1/BLOS1 抗体。
IF 4.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-22 DOI: 10.1042/BCJ20230302
Paramesha Bugga, Michael W Stoner, Janet R Manning, Bellina A S Mushala, Nisha Bhattarai, Maryam Sharifi-Sanjani, Bradley R Webster, Dharendra Thapa, Iain Scott

GCN5L1, also known as BLOC1S1 and BLOS1, is a small intracellular protein involved in many key biological processes. Over the last decade, GCN5L1 has been implicated in the regulation of protein lysine acetylation, energy metabolism, endo-lysosomal function, and cellular immune pathways. An increasing number of published papers have used commercially-available reagents to interrogate GCN5L1 function. However, in many cases these reagents have not been rigorously validated, leading to potentially misleading results. In this report we tested several commercially-available antibodies for GCN5L1, and found that two-thirds of those available did not unambiguously detect the protein by western blot in cultured mouse cells or ex vivo liver tissue. These data suggest that previously published studies which used these unverified antibodies to measure GCN5L1 protein abundance, in the absence of other independent methods of corroboration, should be interpreted with appropriate caution.

GCN5L1又称BLOC1S1和BLOS1,是一种细胞内小蛋白,参与了许多关键的生物过程。在过去十年中,GCN5L1 与蛋白质赖氨酸乙酰化、能量代谢、内溶酶体功能和细胞免疫途径的调控有关。越来越多已发表的论文使用市售试剂来检测 GCN5L1 的功能。然而,在许多情况下,这些试剂并没有经过严格的验证,可能会导致误导性的结果。在本报告中,我们测试了几种市售的 GCN5L1 抗体,发现三分之二的抗体在培养的小鼠细胞或体内外肝脏组织中不能通过 Western 印迹明确检测到该蛋白。这些数据表明,在没有其他独立方法证实的情况下,以前发表的使用这些未经验证的抗体来测量 GCN5L1 蛋白丰度的研究应该谨慎解读。
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引用次数: 0
Ring finger protein 138 inhibits transcription factor C/EBPα protein turnover leading to differentiation arrest in acute myeloid leukemia. RNF138 可抑制转录因子 C/EBPα 蛋白的周转,导致急性髓细胞性白血病的分化停滞。
IF 4.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-22 DOI: 10.1042/BCJ20240027
Anil Kumar Singh, Vishal Upadhyay, Arppita Sethi, Sangita Chowdhury, Shivkant Mishra, Shailendra Prasad Verma, Madan Lal Brahma Bhatt, Arun Kumar Trivedi

E3 ubiquitin ligase, ring finger protein 138 (RNF138) is involved in several biological processes; however, its role in myeloid differentiation or tumorigenesis remains unclear. RNAseq data from TNMplot showed that RNF138 mRNA levels are highly elevated in acute myeloid leukemia (AML) bone marrow samples as compared with bone marrow of normal volunteers. Here, we show that RNF138 serves as an E3 ligase for the tumor suppressor CCAAT/enhancer binding protein (C/EBPα) and promotes its degradation leading to myeloid differentiation arrest in AML. Wild-type RNF138 physically interacts with C/EBPα and promotes its ubiquitin-dependent proteasome degradation while a mutant RNF-138 deficient in ligase activity though interacts with C/EBPα, fails to down-regulate it. We show that RNF138 depletion enhances endogenous C/EBPα levels in peripheral blood mononuclear cells (PBMCs) isolated from healthy volunteers. Our data further shows that RNF138-mediated degradation of C/EBPα negatively affects its transactivation potential on its target genes. Furthermore, RNF138 overexpression inhibits all-trans-retinoic acid-induced differentiation of HL-60 cells whereas RNF138 RNAi enhances. In line with RNF138 inhibiting C/EBPα protein turnover, we also observed that RNF138 overexpression inhibited β-estradiol (E2)-induced C/EBPα driven granulocytic differentiation in C/EBPα inducible K562-p42C/EBPα-estrogen receptor cells. Furthermore, we also recapitulated these findings in PBMCs isolated from AML patients where depletion of RNF138 increased the expression of myeloid differentiation marker CD11b. These results suggest that RNF138 inhibits myeloid differentiation by targeting C/EBPα for proteasomal degradation and may provide a plausible mechanism for loss of C/EBPα expression often observed in myeloid leukemia. Also, targeting RNF138 may resolve differentiation arrest by restoring C/EBPα expression in AML.

E3泛素连接酶环指蛋白138(RNF138)参与多种生物过程,但它在髓细胞分化或肿瘤发生中的作用仍不清楚。TNMplot 的 RNAseq 数据显示,与正常志愿者的骨髓相比,急性髓性白血病(AML)骨髓样本中的 RNF138 mRNA 水平高度升高。在这里,我们发现RNF138是肿瘤抑制因子CCAAT/增强子结合蛋白(C/EBPα)的E3连接酶,可促进其降解,从而导致急性髓细胞白血病患者的髓细胞分化停滞。野生型RNF138与C/EBPα发生物理作用,促进其泛素依赖性蛋白酶体降解,而缺乏连接酶活性的突变体RNF-138虽然与C/EBPα发生作用,但却不能下调C/EBPα。我们的研究表明,在从健康志愿者体内分离出的 PBMCs 中,RNF138 的缺失会提高内源性 C/EBPα 的水平。我们的数据进一步表明,RNF138 介导的 C/EBPα 降解会对其靶基因的转录潜能产生负面影响。此外,RNF138 的过表达抑制了 ATRA 诱导的 HL-60 细胞分化,而 RNF138 RNAi 则增强了分化。与RNF138抑制C/EBPα蛋白周转相一致,我们还观察到,在C/EBPα诱导的K562-p42C/EBPα-雌激素受体(ER)细胞中,RNF138过表达抑制了β-雌二醇(E2)诱导的C/EBPα驱动的粒细胞分化。此外,我们还在分离自 AML 患者的 PBMCs 中重现了这些发现,其中 RNF138 的耗竭会增加髓系分化标记 CD11b 的表达。这些结果表明,RNF138 通过靶向蛋白酶体降解 C/EBPα 来抑制髓系分化,这可能为髓性白血病中经常观察到的 C/EBPα 表达缺失提供了一种合理的机制。此外,靶向 RNF138 可通过恢复 C/EBPα 在急性髓细胞白血病中的表达来解决分化停滞问题。
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引用次数: 0
Correction: The uncharacterized Pseudomonas aeruginosa PA4189 is a novel and efficient aminoacetaldehyde dehydrogenase. 更正:未定性的铜绿假单胞菌 PA4189 是一种新型高效的氨基乙醛脱氢酶。
IF 4.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-22 DOI: 10.1042/BCJ20220567_COR
Arline Fernández-Silva Ana L Juárez-Vázquez Lilian González-Segura Javier Andrés Juárez-Díaz Rosario A Muñoz-Clares
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引用次数: 0
Expression of neuronal NO synthase α- and β-isoforms in skeletal muscle of mice 小鼠骨骼肌中神经元 NO 合酶 α 和 β 异构体的表达
IF 4.1 3区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-08 DOI: 10.1042/bcj20230458
Baum, Oliver
Knowledge of the primary structure of neuronal NO synthase (nNOS) in skeletal muscle is still conflicting and needs further clarification. To elucidate the expression patterns of nNOS isoforms at both mRNA and protein level, systematic reverse transcription (RT)-PCR and epitope mapping by qualitative immunoblot analysis on skeletal muscle of C57/BL6 mice were performed. The ability of the nNOS isoforms to form aggregates was characterized by native low-temperature polyacrylamide electrophoresis (LT-PAGE). The molecular analysis was focused on the rectus femoris (RF) muscle, a skeletal muscle with a nearly balanced ratio of nNOS α- and β-isoforms. RT-PCR amplificates from RF muscles showed exclusive exon-1d mRNA expression, either with or without exon-μ. Epitope mapping demonstrated the simultaneous expression of the nNOS splice variants α/μ, α/non-μ, β/μ and β/non-μ. Furthermore, immunoblotting suggests that the transition between nNOS α- and β-isoforms lies within exon-3. In LT-PAGE, three protein nNOS associated aggregates were detected in homogenates of RF muscle and tibialis anterior muscle: a 320 kDa band containing nNOS α-isoforms, while 250 and 300 kDa bands consist of nNOS β-isoforms that form homodimers or heterodimers with non-nNOS proteins.
人们对骨骼肌中神经元 NO 合酶(nNOS)的主要结构的认识仍然存在冲突,需要进一步澄清。为了阐明 nNOS 同工酶在 mRNA 和蛋白质水平上的表达模式,研究人员对 C57/BL6 小鼠的骨骼肌进行了系统的反转录 (RT)-PCR 分析,并通过定性免疫印迹分析绘制了表位图。通过原生低温聚丙烯酰胺电泳(LT-PAGE)鉴定了 nNOS 异构体形成聚集体的能力。分子分析的重点是股直肌,这是一种 nNOS α 和 β 异构体比例几乎平衡的骨骼肌。来自 RF 肌肉的 RT-PCR 扩增片段显示了外显子-1d mRNA 的独家表达,有的有外显子-μ,有的没有外显子-μ。外显子图谱显示,nNOS剪接变体α/μ、α/non-μ、β/μ和β/non-μ同时表达。此外,免疫印迹表明,nNOS α 和 β 异构体之间的转换位于外显子 3 中。在 LT-PAGE 中,在射频肌肉和胫骨前肌的匀浆中检测到三种与 nNOS 相关的蛋白聚集体:320 kDa 的条带含有 nNOS α-异构体,而 250 和 300 kDa 的条带由 nNOS β-异构体组成,它们与非 nNOS 蛋白形成同二聚体或异二聚体。
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引用次数: 0
Biochemical and structural impact of two novel missense mutations in cystathionine β-synthase gene associated with homocystinuria. 与高胱氨酸尿症相关的胱硫醚-β-合成酶基因中两种新型错义突变的生化和结构影响。
IF 4.1 3区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-24 DOI: 10.1042/BCJ20240012
Duaa W Al-Sadeq, Carolina Conter, Angelos Thanassoulas, Nader Al-Dewik, Bared Safieh-Garabedian, Luis Alfonso Martínez-Cruz, Gheyath K Nasrallah, Alessandra Astegno, Michail Nomikos

Homocystinuria is a rare disease caused by mutations in the CBS gene that results in a deficiency of cystathionine β-synthase (CBS). CBS is an essential pyridoxal 5'-phosphate (PLP)-dependent enzyme in the transsulfuration pathway, responsible for combining serine with homocysteine to produce cystathionine, whose activity is enhanced by the allosteric regulator S-adenosylmethionine (SAM). CBS also plays a role in generating hydrogen sulfide (H2S), a gaseous signaling molecule with diverse regulatory functions within the vascular, nervous, and immune systems. In this study, we present the clinical and biochemical characterization of two novel CBS missense mutations that do not respond to pyridoxine treatment, namely c.689T > A (L230Q) and 215A > T (K72I), identified in a Chinese patient. We observed that the disease-associated K72I genetic variant had no apparent effects on the spectroscopic and catalytic properties of the full-length enzyme. In contrast, the L230Q variant expressed in Escherichia coli did not fully retain heme and when compared with the wild-type enzyme, it exhibited more significant impairments in both the canonical cystathionine-synthesis and the alternative H2S-producing reactions. This reduced activity is consistent with both in vitro and in silico evidence, which indicates that the L230Q mutation significantly decreases the overall protein's stability, which in turn, may represent the underlying cause of its pathogenicity.

同型半胱氨酸尿症是一种罕见疾病,由 CBS 基因突变引起,导致胱硫醚 β 合成酶(CBS)缺乏。CBS 是转硫化途径中一种重要的依赖吡哆醛-5'-磷酸(PLP)的酶,负责将丝氨酸与同型半胱氨酸结合生成胱硫醚,其活性在异构调节剂 S-腺苷蛋氨酸(SAM)的作用下得到增强。CBS 还在生成硫化氢(H2S)中发挥作用,硫化氢是一种气态信号分子,在血管、神经和免疫系统中具有多种调节功能。在这项研究中,我们介绍了在一名中国患者身上发现的两种对吡哆醇治疗无效的新型 CBS 错义突变(即 c.689T>A (L230Q) 和 215A>T (K72I))的临床和生化特征。我们观察到,与疾病相关的 K72I 基因变异对全长酶的光谱和催化特性没有明显影响。相反,在大肠杆菌中表达的 L230Q 变体不能完全保留血红素,与野生型酶相比,它在典型的胱硫醚合成和替代的 H2S 生成反应中都表现出更明显的缺陷。这种活性的降低与体外和硅学证据一致,表明 L230Q 突变显著降低了整个蛋白质的稳定性,这反过来又可能是其致病性的根本原因。
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引用次数: 0
AMP-activated protein kinase can be allosterically activated by ADP but AMP remains the key activating ligand AMP 激活的蛋白激酶可被 ADP 异源激活,但 AMP 仍是关键的激活配体
IF 4.1 3区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-24 DOI: 10.1042/bcj20240082
Hawley, Simon A., Russell, Fiona M., Hardie, D. Grahame
The AMP-activated protein kinase (AMPK) is a sensor of cellular energy status. When activated by increases in ADP:ATP and/or AMP:ATP ratios (signalling energy deficit), AMPK acts to restore energy balance. Binding of AMP to one or more of three CBS repeats (CBS1, CBS3, CBS4) on the AMPK-γ subunit activates the kinase complex by three complementary mechanisms: (i) promoting α-subunit Thr172 phosphorylation by the upstream kinase LKB1; (ii) protecting against Thr172 dephosphorylation; (iii) allosteric activation. Surprisingly, binding of ADP has been reported to mimic the first two effects, but not the third. We now show that at physiologically relevant concentrations of Mg.ATP2− (above those used in the standard assay) ADP binding does cause allosteric activation. However, ADP causes only a modest activation because (unlike AMP), at concentrations just above those where activation becomes evident, ADP starts to cause competitive inhibition at the catalytic site. Our results cast doubt on the physiological relevance of the effects of ADP and suggest that AMP is the primary activator in vivo. We have also made mutations to hydrophobic residues involved in binding adenine nucleotides at each of the three γ subunit CBS repeats of the human α2β2γ1 complex and examined their effects on regulation by AMP and ADP. Mutation of the CBS3 site has the largest effects on all three mechanisms of AMP activation, especially at lower ATP concentrations, while mutation of CBS4 reduces the sensitivity to AMP. All three sites appear to be required for allosteric activation by ADP.
AMP激活蛋白激酶(AMPK)是细胞能量状态的传感器。当ADP:ATP和/或AMP:ATP比率增加时(能量不足信号),AMPK被激活,从而恢复能量平衡。AMPK-γ 亚基上的三个 CBS 重复序列(CBS1、CBS3、CBS4)中的一个或多个与 AMPK 结合,通过三种互补机制激活激酶复合物:(i) 通过上游激酶 LKB1 促进 α 亚基 Thr172 磷酸化;(ii) 防止 Thr172 去磷酸化;(iii) 异位激活。令人惊讶的是,据报道结合 ADP 可模拟前两种效应,但不能模拟第三种效应。我们现在的研究表明,在 Mg.ATP2- 的生理相关浓度下(高于标准测定中使用的浓度),ADP 结合确实会导致异源活化。然而,ADP 只引起适度的活化,因为(与 AMP 不同)在浓度刚刚超过活化变得明显时,ADP 开始在催化位点引起竞争性抑制。我们的结果使人对 ADP 作用的生理相关性产生怀疑,并表明 AMP 才是体内的主要激活剂。我们还对人α2β2γ1复合体的三个γ亚基 CBS 重复位点上参与结合腺嘌呤核苷酸的疏水残基进行了突变,并研究了它们对 AMP 和 ADP 调节的影响。CBS3 位点的突变对所有三种 AMP 激活机制的影响最大,尤其是在较低的 ATP 浓度下,而 CBS4 的突变则降低了对 AMP 的敏感性。这三个位点似乎都是 ADP 异源激活所必需的。
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