更新于：2024-11-01

COTL1

更新于：2024-11-01

基本信息

别名

CLP、coactosin like F-actin binding protein 1、Coactosin-like protein

+ [1]

简介

Binds to F-actin in a calcium-independent manner. Has no direct effect on actin depolymerization. Acts as a chaperone for ALOX5 (5LO), influencing both its stability and activity in leukotrienes synthesis.

关联

100 项与 COTL1 相关的临床结果

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100 项与 COTL1 相关的转化医学

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0 项与 COTL1 相关的专利（医药）

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项与 COTL1 相关的文献（医药）

2024-12-01·Molecular Genetics and Genomics

A novel imprinted locus on bovine chromosome 18 homologous with human chromosome 16q24.1

Article

作者: Zhang, Yinjiao ; Huo, Haonan ; Wang, Kun ; Li, Shujing ; Li, Shijie ; Chen, Weina ; Zhang, Cui ; Wang, Siwei ; Yu, Wenli

Genomic imprinting is an epigenetic regulation mechanism in mammals resulting in the parentally dependent monoallelic expression of genes. Imprinting disorders in humans are associated with several congenital syndromes and cancers and remain the focus of many medical studies. Cattle is a better model organism for investigating human embryo development than mice. Imprinted genes usually cluster on chromosomes and are regulated by different methylation regions (DMRs) located in imprinting control regions that control gene expression in cis. There is an imprinted locus on human chromosome 16q24.1 associated with congenital lethal developmental lung disease in newborns. However, genomic imprinting on bovine chromosome 18, which is homologous with human chromosome 16 has not been systematically studied. The aim of this study was to analyze the allelic expressions of eight genes (CDH13, ATP2C2, TLDC1, COTL1, CRISPLD2, ZDHHC7, KIAA0513, and GSE1) on bovine chromosome 18 and to search the DMRs associated gene allelic expression. Three transcript variants of the ZDHHC7 gene (X1, X2, and X5) showed maternal imprinting in bovine placentas. In addition, the monoallelic expression of X2 and X5 was tissue-specific. Five transcripts of the KIAA0513 gene showed tissue- and isoform-specific monoallelic expression. The CDH13, ATP2C2, and TLDC1 genes exhibited tissue-specific imprinting, however, COTL1, CRISLPLD2, and GSE1 escaped imprinting. Four DMRs, established after fertilization, were found in this region. Two DMRs were located between the ZDHHC7 and KIAA0513 genes, and two were in exon 1 of the CDH13 and ATP2C2 genes, respectively. The results from this study support future studies on the molecular mechanism to regulate the imprinting of candidate genes on bovine chromosome 18.

2024-10-01·Cell Host & Microbe

Networks of human milk microbiota are associated with host genomics, childhood asthma, and allergic sensitization

Article

作者: Stickley, Sara A. ; Turvey, Stuart E ; Zacharias, Amanda M. ; Azad, Meghan B ; Moossavi, Shirin ; Fang, Zhi Yi ; Fehr, Kelsey ; Miliku, Kozeta ; Subbarao, Padmaja ; Surette, Michael G. ; Petersen, Charisse ; Sears, Malcolm R. ; Zacharias, Amanda M ; Ambalavanan, Amirthagowri ; Moraes, Theo J ; Zhang, Yang ; Stickley, Sara A ; Simons, Elinor ; Azad, Meghan B. ; Duan, Qingling ; Sears, Malcolm R ; Turvey, Stuart E. ; Mandhane, Piushkumar J ; Mandhane, Piushkumar J. ; Moraes, Theo J. ; Surette, Michael G

The human milk microbiota (HMM) is thought to influence the long-term health of offspring. However, its role in asthma and atopy and the impact of host genomics on HMM composition remain unclear. Through the CHILD Cohort Study, we followed 885 pregnant mothers and their offspring from birth to 5 years and determined that HMM was associated with maternal genomics and prevalence of childhood asthma and allergic sensitization (atopy) among human milk-fed infants. Network analysis identified modules of correlated microbes in human milk that were associated with subsequent asthma and atopy in preschool-aged children. Moreover, reduced alpha-diversity and increased Lawsonella abundance in HMM were associated with increased prevalence of childhood atopy. Genome-wide association studies (GWASs) identified maternal genetic loci (e.g., ADAMTS8, NPR1, and COTL1) associated with HMM implicated with asthma and atopy, notably Lawsonella and alpha-diversity. Thus, our study elucidates the role of host genomics on the HMM and its potential impact on childhood asthma and atopy.

2024-05-30·Aging

Potential marker genes for chronic obstructive pulmonary disease revealed based on single-cell sequencing and Mendelian randomization analysis

Article

作者: Zhou, Yun ; Huang, Lewei ; Song, Di ; Yu, Shuo ; Ma, Feifei ; Che, Xiangqian ; Han, Xiaoxiao ; Sun, Gang

BACKGROUNDProgress is being made in the prevention and treatment of chronic obstructive pulmonary disease (COPD), but it is still unsatisfactory. With the development of genetic technology, validated genetic information can better explain COPD.OBJECTIVEThe study utilized scRNA-seq and Mendelian randomization analysis of eQTLs to identify crucial genes and potential mechanistic pathways underlying COPD pathogenesis.MEHODSSingle-cell sequencing data were used to identify marker genes for immune cells in the COPD process. Data on eQTLs for immune cell marker genes were obtained from the eQTLGen consortium. To estimate the causal effect of marker genes on COPD, we selected an independent cohort (ukb-b-16751) derived from the UK Biobank database for two-sample Mendelian randomization analysis. Subsequently, we performed immune infiltration analysis, gene set enrichment analysis (GSEA), and co-expression network analysis on the key genes.RESULTSThe 154 immune cell-associated marker genes identified were mainly involved in pathways such as vacuolar cleavage, positive regulation of immune response and regulation of cell activation. Mendelian randomization analysis screened four pairs of marker genes (GZMH, COTL1, CSTA and CD14) were causally associated with COPD. These four key genes were significantly associated with immune cells. In addition, we have identified potential transcription factors associated with these key genes using the Cistrome database, thus contributing to a deeper understanding of the regulatory network of these gene expressions.CONCLUSIONSThis eQTLs Mendelian randomization study identified four key genes (GZMH, COTL1, CSTA, and CD14) causally associated with COPD, providing new insights for prevention and treatment of COPD.