更新于：2024-11-01

CYB5B

更新于：2024-11-01

基本信息

别名

CYB5-M、CYB5B、CYB5M

+ [3]

简介

Cytochrome b5 is a membrane-bound hemoprotein functioning as an electron carrier for several membrane-bound oxygenases.

关联

100 项与 CYB5B 相关的临床结果

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100 项与 CYB5B 相关的转化医学

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0 项与 CYB5B 相关的专利（医药）

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103

项与 CYB5B 相关的文献（医药）

2024-03-05·Reviews in Cardiovascular Medicine

Metformin Therapeutic Targets for Aortic Aneurysms: A Mendelian Randomization and Colocalization Study

Article

作者: Zhang, Dingkai ; Zhang, Zhaohua ; Wen, Jianyan ; Gao, Xixi ; Ye, Zhidong ; Yang, Liang ; Xu, Mingyuan ; Liu, Peng ; Liu, Jingwen ; Ni, Bin

BackgroundIdentifying effective pharmacological interventions to prevent the progressive enlargement and rupture of aortic aneurysms (AAs) is critical. Previous studies have suggested links between metformin use and a decreased incidence of AAs. In this study, we employed Mendelian randomization (MR) to investigate causal effects of metformin's targets on AA risk and to explore the underlying mechanisms underlying these effects.MethodsTo examine the relationship between metformin use and AA risk, we implemented both two-sample MR and multivariable MR analyses. Utilizing genetic instrumental variables, we retrieved cis-expression quantitative trait loci (cis-eQTL) data for potential targets of metformin from the Expression Quantitative Trait Loci Genetics Consortium (eQTLGen) Consortium and Genotype-Tissue Expression (GTEx) project. Colocalization analysis was employed to ascertain the probability of shared causal genetic variants between single nucleotide polymorphisms (SNPs) associated with eQTLs and AA.ResultsOur findings reveal that metformin use reduces AA risk, exhibiting a protective effect with an odds ratio (OR) of 4.88 __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__× __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__10 - 3 (95% confidence interval [CI]: 7.30 __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__× __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__10 - 5 -0.33, p = 0.01). Furthermore, the protective effect of type 2 diabetes on AA risk appears to be driven by metformin use ( __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__OR MVMR = 1.34 __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__× __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__10 - 4 , 95% CI: 3.97 __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__× __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__10 - 8 -0.45, p = 0.03). Significant Mendelian randomization (MR) results were observed for the expression of two metformin-related genes in the bloodstream: NADH:ubiquinone oxidoreductase subunit A6 (NDUFA6) and cytochrome b5 type B (CYB5B), across two independent datasets ( __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__OR CYB5B = 1.35, 95% CI: 1.20-1.51, p = 2.41 __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__× __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__10 - 7 ; __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__OR NDUFA6 = 1.12; 95% CI: 1.07-1.17, p = 1.69 __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__× __-mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"-__10 - 6 ). The MR analysis of tissue-specific expression also demonstrated a positive correlation between increased NDUFA6 expression and heightened AA risk. Lastly, NDUFA6 exhibited evidence of colocalization with AA.ConclusionsOur study suggests that metformin may play a significant role in lowering the risk of AA. This protective effect could potentially be linked to the mitigation of mitochondrial and immune dysfunction. Overall, NDUFA6 has emerged as a potential mechanism through which metformin intervention may confer AA protection.

2024-02-16·Microbiology

Identification of novel tail-anchored membrane proteins integrated by the bacterial twin-arginine translocase

Article

作者: Chandra, Govind ; Severi, Emmanuele ; Palmer, Tracy ; Gallego-Parrilla, José Jesús

The twin-arginine protein transport (Tat) system exports folded proteins across the cytoplasmic membranes of prokaryotes and the energy transducing-membranes of plant thylakoids and mitochondria. Proteins are targeted to the Tat machinery by N-terminal signal peptides with a conserved twin-arginine motif, and some substrates are exported as heterodimers where the signal peptide is present on one of the partner proteins. A subset of Tat substrates is found in the membrane. Tat-dependent membrane proteins usually have large globular domains and a single transmembrane helix present at the N- or C-terminus. Five Tat substrates that have C-terminal transmembrane helices have previously been characterized in the model bacterium Escherichia coli. Each of these is an iron–sulfur cluster-containing protein involved in electron transfer from hydrogen or formate. Here we have undertaken a bioinformatic search to identify further tail-anchored Tat substrates encoded in bacterial genomes. Our analysis has revealed additional tail-anchored iron–sulfur proteins associated in modules with either a b-type cytochrome or a quinol oxidase. We also identified further candidate tail-anchored Tat substrates, particularly among members of the actinobacterial phylum, that are not predicted to contain cofactors. Using reporter assays, we show experimentally that six of these have both N-terminal Tat signal peptides and C-terminal transmembrane helices. The newly identified proteins include a carboxypeptidase and a predicted protease, and four sortase substrates for which membrane integration is a prerequisite for covalent attachment to the cell wall.

2023-09-01·iScience

LINC00116-encoded microprotein mitoregulin regulates fatty acid metabolism at the mitochondrial outer membrane

Article

作者: Kappei, Dennis ; Guo, Yabo ; Yen, Paul ; Xu, He ; Bichler, Zoë ; Wu, Gaoqi ; Zhang, Shan ; Ho, Lena ; Guo, Ruiyang ; Singh, Brijesh K ; Robinson, David R L ; Fidelito, Gio ; Zhou, Quan D ; Stroud, David A ; Lim, Radiance ; Liang, Chao

LINC00116 encodes a microprotein first identified as Mitoregulin (MTLN), where it was reported to localize to the inner membrane of mitochondria to regulate fatty acid oxidation and oxidative phosphorylation. These initial discoveries were followed by reports with differing findings about its molecular functions and submitochondrial localization. To clarify the apparent discrepancies, we constructed multiple orthogonal methods of determining the localization of MTLN, including split GFP-based reporters that enable efficient and reliable topology analyses for microproteins. These methods unequivocally demonstrate MTLN primarily localizes to the outer membrane of mitochondria, where it interacts with enzymes of fatty acid metabolism including CPT1B and CYB5B. Loss of MTLN causes the accumulation of very long-chain fatty acids (VLCFAs), especially docosahexaenoic acid (DHA). Intriguingly, loss of MTLN protects mice against western diet/fructose-induced insulin-resistance, suggests a protective effect of VLCFAs in this context. MTLN thus serves as an attractive target to control the catabolism of VLCFAs.