Ask about this productRelated genes to: CYB5D1 antibody
- Gene:
- CYB5D1 NIH gene
- Name:
- cytochrome b5 domain containing 1
- Previous symbol:
- -
- Synonyms:
- FLJ32499
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-12
- Date modifiied:
- 2015-08-28
Related products to: CYB5D1 antibody
Related articles to: CYB5D1 antibody
- Coordinated ciliary/flagellar beating requires precise spatiotemporal regulation of molecular motors such as dyneins, yet the molecular mechanisms governing ciliary synchrony remain poorly understood. Here, we demonstrate that a heme-binding axonemal protein CYB5D1 functions as a redox-sensitive switch that controls flagellar beating coordination by regulating Ca dynamics. Both the D58G point mutation, which abolishes heme-binding activity, and the complete loss of CYB5D1 lead to a reduction in the flagellar redox potential. More importantly, the hyperreductive intraflagellar redox shift in the mutant increases -flagellar Ca spike frequency and amplitude, similar to reductive treatment of wild-type flagella, resulting in the loss of flagellar beating coordination. Interestingly, oxidative treatments induced synchronized Ca spikes across both - and -flagella of and increased flagellar beating coordination. In addition, loss of CYB5D1 raised the intraflagellar Ca pool. These results indicate that CYB5D1 links redox sensing to Ca signaling in ciliary coordination and reveal how the two flagella of the same cell achieve synchronized beating through redox-gated Ca dynamics. Furthermore, CYB5D1 loss impairs gliding motility by dysregulating Ca spiking specifically in the leading flagellum, extending the redox-Ca regulatory axis to surface-associated flagellar behaviors. Given the evolutionary conservation of both CYB5D1 and the redox-Ca signaling axis, this mechanism likely regulates ciliary function across eukaryotes, with implications for understanding ciliopathies and respiratory diseases. - Source: PubMed
Publication date: 2026/08/19
Lin YiwenZhao LijuanLiu GaiDeng XuanKing Stephen MHuang Kaiyao - Older patients are at risk for acute kidney injury and chronic kidney disease. Age-related increases in DNA methylation at CpG islands have been linked to aging-related diseases like cancer and cardiovascular disease, but the exact causal relationship between methylation in renal aging and other kidney diseases remains unclear. This study aimed to elucidate the methylation status of peripheral blood mononuclear cells (PBMCs) in the Asian population. Using human whole blood DNA methylation analysis from the Taiwan Biobank, we included participants with both whole blood genome-wide methylation data and follow-up data on serum creatinine. We investigated hyper- and hypomethylated genes in comparison of participants with higher and lower estimated glomerular filtration (eGFR) decline rate in overall cohort as well as in comparison of old and young participants in subgroup of participants with higher eGFR decline rate. Common genes and signaling pathways in both comparative analyses were identified. - Source: PubMed
Publication date: 2024/06/15
Yang Po-LungLai Tai-ShuanChou Yu-HsiangLai Liang-ChuanLin Shuei-LiongChen Yung-Ming - Coordinated beating is crucial for the function of multiple cilia. However, the molecular mechanism is poorly understood. Here, we characterize a conserved ciliary protein CYB5D1 with a heme-binding domain and a cordon-bleu ubiquitin-like domain. Mutation or knockdown of in zebrafish impaired coordinated ciliary beating in the otic vesicle and olfactory epithelium. Similarly, the two flagella of an insertional mutant of the CYB5D1 ortholog in () showed an uncoordinated pattern due to a defect in the -flagellum. Biochemical analyses revealed that CrCYB5D1 is a radial spoke stalk protein that binds heme only under oxidizing conditions. Lack of CrCYB5D1 resulted in a reductive shift in flagellar redox state and slowing down of the phototactic response. Treatment of with oxidants restored coordinated flagellar beating. Taken together, these data suggest that CrCYB5D1 may integrate environmental and intraciliary signals and regulate the redox state of cilia, which is crucial for the coordinated beating of multiple cilia. - Source: PubMed
Zhao LijuanXie HaiboKang YunsiLin YiwenLiu GaiSakato-Antoku MihoPatel-King Ramila SWang BingWan CuihongKing Stephen MZhao ChengtianHuang Kaiyao - Characterization of genetic variants affecting genome-wide gene expression levels (expression quantitative trait loci or eQTLs) in pig testes may improve our understanding of genetic architecture of boar taint (an animal welfare trait) and helps in genome-assisted or genomic selection programs. The aims of this study were to identify eQTLs associated with androstenone, to find candidate eQTLs for low androstenone, and to validate the top eQTL by reverse transcriptase quantitative PCR (RT-qPCR). Gene expression profiles were obtained by RNA sequencing in testis from Danish cross-bred pigs and genotype data by 80K single nucleotide polymorphism panel. A total of 262 eQTLs [false discovery rate (FDR) < 0.05] were identified by using two software packages: Matrix eQTL and Krux eQTL. Of these, 149 -acting eQTLs were significantly associated with androstenone concentrations and gene expression (FDR < 0.05). The eQTLs were associated with several genes of boar taint relevance including and . One eQTL gene, , was differentially expressed (FDR < 0.05) and affected by chicory. Five candidate eQTLs associated with low androstenone concentrations were discovered, including the top eQTL associated with . RT-qPCR confirmed target gene expression to be significantly ( < 0.05) different based on eQTL genotypes. Furthermore, eQTLs were enriched as QTLs for 15 boar taint related traits from the PigQTLdb. This is the first study to report eQTLs in testes of commercial crossbred pigs used in pork production and to reveal genetic architecture of boar taint. Potential applications include development of a DNA test and in advanced genomic selection models for boar taint. - Source: PubMed
Publication date: 2019/08/02
Drag Markus HKogelman Lisette J AMaribo HanneMeinert LeneThomsen Preben DKadarmideen Haja N - Zinc oxide nanoparticles (ZnO NPs) are being utilized in an increasing number of fields and commercial applications. While their general toxicity and associated oxidative stress have been extensively studied, the toxicological pathways that they induce in developmental stages are still largely unknown. In this study, the developmental toxicity of ZnO NPs to embryonic/larval zebrafish was investigated. The transcriptional expression profiles induced by ZnO NPs were also investigated to ascertain novel genomic responses related to their specific toxicity pathway. Zebrafish embryos were exposed to 0.01, 0.1, 1, and 10 mg/L ZnO NPs for 96 h post-fertilization. The toxicity of ZnO NPs, based on their Zn concentration, was quite similar to that in embryonic/larval zebrafish exposed to corresponding ZnSO4 concentrations. Pericardial edema and yolk-sac edema were the principal malformations induced by ZnO NPs. Gene-expression profiling using microarrays demonstrated 689 genes that were differentially regulated (fold change >1.5) following exposure to ZnO NPs (498 upregulated, 191 downregulated). Several genes that were differentially regulated following ZnO NP exposure shared similar biological pathways with those observed with ZnSO4 exposure, but six genes (aicda, cyb5d1, edar, intl2, ogfrl2 and tnfsf13b) associated with inflammation and the immune system responded specifically to ZnO NPs (either in the opposite direction or were unchanged in ZnSO4 exposure). Real-time reverse-transcription quantitative polymerase chain reaction confirmed that the responses of these genes to ZnO NPs were significantly different from their response to ZnSO4 exposure. ZnO NPs may affect genes related to inflammation and the immune system, resulting in yolk-sac edema and pericardia edema in embryonic/larval developmental stages. These results will assist in elucidating the mechanisms of toxicity of ZnO NPs during development of zebrafish. - Source: PubMed
Publication date: 2016/08/09
Choi Jin SooKim Ryeo-OkYoon SeokjooKim Woo-Keun