Essays in biochemistry最新文献_第3页

Sulfation pathways in the maintenance of functional beta-cell mass and implications for diabetes. 维持功能性β细胞质量的硫酸化途径及其对糖尿病的影响。

IF 5.6 2区生物学

Essays in biochemistry Pub Date : 2024-12-04 DOI: 10.1042/EBC20240034

Jonathan Wolf Mueller, Patricia Thomas, Louise Torp Dalgaard, Gabriela da Silva Xavier

{"title":"Sulfation pathways in the maintenance of functional beta-cell mass and implications for diabetes.","authors":"Jonathan Wolf Mueller, Patricia Thomas, Louise Torp Dalgaard, Gabriela da Silva Xavier","doi":"10.1042/EBC20240034","DOIUrl":"10.1042/EBC20240034","url":null,"abstract":"Diabetes Type 1 and Type 2 are widely occurring diseases. In spite of a vast amount of biomedical literature about diabetic processes in general, links to certain biological processes are only becoming evident these days. One such area of biology is the sulfation of small molecules, such as steroid hormones or metabolites from the gastrointestinal tract, as well as larger biomolecules, such as proteins and proteoglycans. Thus, modulating the physicochemical propensities of the different sulfate acceptors, resulting in enhanced solubility, expedited circulatory transit, or enhanced macromolecular interaction. This review lists evidence for the involvement of sulfation pathways in the maintenance of functional pancreatic beta-cell mass and the implications for diabetes, grouped into various classes of sulfated biomolecule. Complex heparan sulfates might play a role in the development and maintenance of beta-cells. The sulfolipids sulfatide and sulfo-cholesterol might contribute to beta-cell health. In beta-cells, there are only very few proteins with confirmed sulfation on some tyrosine residues, with the IRS4 molecule being one of them. Sulfated steroid hormones, such as estradiol-sulfate and vitamin-D-sulfate, may facilitate downstream steroid signaling in beta-cells, following de-sulfation. Indoxyl sulfate is a metabolite from the intestine, that causes kidney damage, contributing to diabetic kidney disease. Finally, from a technological perspective, there is heparan sulfate, heparin, and chondroitin sulfate, that all might be involved in next-generation beta-cell transplantation. Sulfation pathways may play a role in pancreatic beta-cells through multiple mechanisms. A more coherent understanding of sulfation pathways in diabetes will facilitate discussion and guide future research.","PeriodicalId":11812,"journal":{"name":"Essays in biochemistry","volume":" ","pages":"509-522"},"PeriodicalIF":5.6,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11625869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Does AMPK bind glycogen in skeletal muscle or is the relationship correlative? AMPK 与骨骼肌中的糖原结合吗？

IF 5.6 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240006

Barnaby P Frankish, Robyn M Murphy

{"title":"Does AMPK bind glycogen in skeletal muscle or is the relationship correlative?","authors":"Barnaby P Frankish, Robyn M Murphy","doi":"10.1042/EBC20240006","DOIUrl":"10.1042/EBC20240006","url":null,"abstract":"Since its discovery over five decades ago, an emphasis on better understanding the structure and functional role of AMPK has been prevalent. In that time, the role of AMPK as a heterotrimeric enzyme that senses the energy state of various cell types has been established. Skeletal muscle is a dynamic, plastic tissue that adapts to both functional and metabolic demands of the human body, such as muscle contraction or exercise. With a deliberate focus on AMPK in skeletal muscle, this review places a physiological lens to the association of AMPK and glycogen that has been established biochemically. It discusses that, to date, no in vivo association of AMPK with glycogen has been shown and this is not altered with interventions, either by physiological or biochemical utilisation of glycogen in skeletal muscle. The reason for this is likely due to the persistent phosphorylation of Thr148 in the β-subunit of AMPK which prevents AMPK from binding to carbohydrate domains. This review presents the correlative data that suggests AMPK senses glycogen utilisation through a direct interaction with glycogen, the biochemical data showing that AMPK can bind carbohydrate in vitro, and highlights that in a physiological setting of rodent skeletal muscle, AMPK does not directly bind to glycogen.","PeriodicalId":11812,"journal":{"name":"Essays in biochemistry","volume":" ","pages":"337-347"},"PeriodicalIF":5.6,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A special issue of Essays in Biochemistry on AMPK and AMPK-related kinases. 关于 AMPK 和 AMPK 相关激酶的《生物化学论文》特刊。

IF 5.6 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240038

Ian P Salt, David Carling

引用次数: 0

New developments in AMPK and mTORC1 cross-talk. AMPK 和 mTORC1 交叉对话的新进展。

IF 8.3 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240007

William J Smiles, Ashley J Ovens, Bruce E Kemp, Sandra Galic, Janni Petersen, Jonathan S Oakhill

{"title":"New developments in AMPK and mTORC1 cross-talk.","authors":"William J Smiles, Ashley J Ovens, Bruce E Kemp, Sandra Galic, Janni Petersen, Jonathan S Oakhill","doi":"10.1042/EBC20240007","DOIUrl":"10.1042/EBC20240007","url":null,"abstract":"Metabolic homeostasis and the ability to link energy supply to demand are essential requirements for all living cells to grow and proliferate. Key to metabolic homeostasis in all eukaryotes are AMPK and mTORC1, two kinases that sense nutrient levels and function as counteracting regulators of catabolism (AMPK) and anabolism (mTORC1) to control cell survival, growth and proliferation. Discoveries beginning in the early 2000s revealed that AMPK and mTORC1 communicate, or cross-talk, through direct and indirect phosphorylation events to regulate the activities of each other and their shared protein substrate ULK1, the master initiator of autophagy, thereby allowing cellular metabolism to rapidly adapt to energy and nutritional state. More recent reports describe divergent mechanisms of AMPK/mTORC1 cross-talk and the elaborate means by which AMPK and mTORC1 are activated at the lysosome. Here, we provide a comprehensive overview of current understanding in this exciting area and comment on new evidence showing mTORC1 feedback extends to the level of the AMPK isoform, which is particularly pertinent for some cancers where specific AMPK isoforms are implicated in disease pathogenesis.","PeriodicalId":11812,"journal":{"name":"Essays in biochemistry","volume":" ","pages":"321-336"},"PeriodicalIF":8.3,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

How mass spectrometry can be exploited to study AMPK. 如何利用质谱技术研究 AMPK。

IF 8.3 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240009

Mark H Rider, Didier Vertommen, Manuel Johanns

引用次数: 0

CaMKK2: bridging the gap between Ca2+ signaling and energy-sensing. CaMKK2：Ca2+信号传导与能量感应之间的桥梁。

IF 5.6 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240011

Luke M McAloon, Abbey G Muller, Kevin Nay, Eudora L Lu, Benoit Smeuninx, Anthony R Means, Mark A Febbraio, John W Scott

{"title":"CaMKK2: bridging the gap between Ca2+ signaling and energy-sensing.","authors":"Luke M McAloon, Abbey G Muller, Kevin Nay, Eudora L Lu, Benoit Smeuninx, Anthony R Means, Mark A Febbraio, John W Scott","doi":"10.1042/EBC20240011","DOIUrl":"10.1042/EBC20240011","url":null,"abstract":"Calcium (Ca2+) ions are ubiquitous and indispensable signaling messengers that regulate virtually every cell function. The unique ability of Ca2+ to regulate so many different processes yet cause stimulus specific changes in cell function requires sensing and decoding of Ca2+ signals. Ca2+-sensing proteins, such as calmodulin, decode Ca2+ signals by binding and modifying the function of a diverse range of effector proteins. These effectors include the Ca2+-calmodulin dependent protein kinase kinase-2 (CaMKK2) enzyme, which is the core component of a signaling cascade that plays a key role in important physiological and pathophysiological processes, including brain function and cancer. In addition to its role as a Ca2+ signal decoder, CaMKK2 also serves as an important junction point that connects Ca2+ signaling with energy metabolism. By activating the metabolic regulator AMP-activated protein kinase (AMPK), CaMKK2 integrates Ca2+ signals with cellular energy status, enabling the synchronization of cellular activities regulated by Ca2+ with energy availability. Here, we review the structure, regulation, and function of CaMKK2 and discuss its potential as a treatment target for neurological disorders, metabolic disease, and cancer.","PeriodicalId":11812,"journal":{"name":"Essays in biochemistry","volume":" ","pages":"309-320"},"PeriodicalIF":5.6,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

New concepts in the roles of AMPK in adipocyte stem cell biology. AMPK 在脂肪干细胞生物学中作用的新概念。

IF 5.6 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240008

Alice E Pollard

{"title":"New concepts in the roles of AMPK in adipocyte stem cell biology.","authors":"Alice E Pollard","doi":"10.1042/EBC20240008","DOIUrl":"10.1042/EBC20240008","url":null,"abstract":"Obesity is a major risk factor for many life-threatening diseases. Adipose tissue dysfunction is emerging as a driving factor in the transition from excess adiposity to comorbidities such as metabolic-associated fatty liver disease, cardiovascular disease, Type 2 diabetes and cancer. However, the transition from healthy adipose expansion to the development of these conditions is poorly understood. Adipose stem cells, residing in the vasculature and stromal regions of subcutaneous and visceral depots, are responsible for the expansion and maintenance of organ function, and are now recognised as key mediators of pathological transformation. Impaired tissue expansion drives inflammation, dysregulation of endocrine function and the deposition of lipids in the liver, muscle and around vital organs, where it is toxic. Contrary to previous hypotheses, it is the promotion of healthy adipose tissue expansion and function, not inhibition of adipogenesis, that presents the most attractive therapeutic strategy in the treatment of metabolic disease. AMP-activated protein kinase, a master regulator of energy homeostasis, has been regarded as one such target, due to its central role in adipose tissue lipid metabolism, and its apparent inhibition of adipogenesis. However, recent studies utilising AMP-activated protein kinase (AMPK)-specific compounds highlight a more subtle, time-dependent role for AMPK in the process of adipogenesis, and in a previously unexplored repression of leptin, independent of adipocyte maturity. In this article, I discuss historic evidence for AMPK-mediated adipogenesis inhibition and the multi-faceted roles for AMPK in adipose tissue.","PeriodicalId":11812,"journal":{"name":"Essays in biochemistry","volume":" ","pages":"349-361"},"PeriodicalIF":5.6,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AMPK and O-GlcNAcylation: interplay in cardiac pathologies and heart failure. AMPK 和 O-GlcNAcylation：心脏病变和心力衰竭中的相互作用。

IF 8.3 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240003

Ettore Vanni, Christophe Beauloye, Sandrine Horman, Luc Bertrand

引用次数: 0

Understanding metabolic plasticity at single cell resolution. 以单细胞分辨率了解代谢可塑性。

IF 5.6 2区生物学

Essays in biochemistry Pub Date : 2024-11-18 DOI: 10.1042/EBC20240002

Christina C Abbate, Jason Hu, John G Albeck

引用次数: 0

NUAK: never underestimate a kinase. NUAK：永远不要低估激酶。