Ask about this productRelated genes to: CMKLR1 antibody
- Gene:
- CMKLR1 NIH gene
- Name:
- chemerin chemokine-like receptor 1
- Previous symbol:
- -
- Synonyms:
- RVER1
- Chromosome:
- 12q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-22
- Date modifiied:
- 2015-04-08
Related products to: CMKLR1 antibody
Related articles to: CMKLR1 antibody
- In mammals, chemerin and its receptor CMKLR1 might be downstream effectors in response to long photoperiod in the ependymal cells lining the third ventricle in rats. Iodothyronine deiodinase 2 (DIO2) is a main product of the involvement of TSH in photoperiodic signaling. Thus, the potential interplay of TSH and Chemerin/CMKLR1 signaling might exist during photoperiodic changes. Our study aimed to investigate whether Chemerin/CMKLR1 signaling could stimulate DIO2 production and how TSH could affect Chemerin/CMKLR1 signaling in primary rat ependymal cells. Colocalization of Chemerin with its receptor, CMKLR1, was observed using immunohistochemistry assay. The expression of chemerin and CMKLR1 was identified using real-time PCR and western blot analysis respectively. DIO2 expression, which involves a dual signaling pathway (an increase in cAMP levels and phosphorylation of ERK1/2, was detected by western blot assay and enzyme-linked immunosorbent assay (ELISA). Our study showed the potential interaction between Chemerin and CMKLR1 in primary rat ependymal cells. TSH could upregulate the expression of chemerin and CMKLR1 in Chemerin-pretreated primary ependymal cells. In vitro treatment of primary ependymal cells with Chemerin (10 ng/mL) or TSH (60 mIU/mL) could induce an increase in cAMP levels, ERK1/2 phosphorylation and DIO2 expression. Furthermore, we found that TSH could promote the effect of Chemerin/CMKLR1 signaling on DIO2 production through an increase in cAMP level and the phosphorylation of ERK1/2. We concluded that Chemerin/CMKLR1 signaling could enhance DIO2 activity in primary rat ependymal cells in vitro, and this effect could be promoted by TSH through cAMP and phosphorylation of ERK1/2. - Source: PubMed
Publication date: 2026/05/12
Ning XinGuo DoudouHuang QingWang CencenLi YatingZhou YanfenLi Xin - - Source: PubMed
Publication date: 2026/04/24
- Hybridization effectively enhances breeding efficiency and significantly boosts sheep productivity. However, the epigenetic mechanisms underlying the superior production performance of crossbreds remain largely elusive. In this study, Hu sheep were crossbred with Suffolk rams used as the paternal line. We integrated RNA-seq, ATAC-seq, and CUT&Tag (H3K4me3, H3K4me1, H3K27ac, and H3K27me3) techniques to characterize epigenetic regulatory differences in the longissimus dorsi muscle between Hu sheep (HU) and crossbred progeny (SH). Phenotypic and transcriptomic analyses revealed that SH crossbred sheep exhibited superior growth performance ( < 0.05), and the upregulated genes in the Apelin signaling pathway were significantly correlated with eye muscle area ( < 0.05). Utilizing a Hidden Markov Model, we annotated 15 distinct chromatin states in both HU and SH sheep, systematically characterizing the dynamic epigenomic landscapes across the two breeds. In contrast to SH sheep, the genome of HU sheep exhibited enrichment of repressive chromatin modifications typified by H3K27me3. Strong active enhancers (EnhA) were significantly enriched within upregulated genes in SH. A total of 1862 SH-specific and 691 HU-specific EnhA elements were characterized in this study. Motif analysis revealed that SH-specific EnhA were enriched for myogenic MEF2 family motifs ( < 0.05), which promote muscle and vascular development. By integrating multi-omics data, we constructed a putative regulatory network potentially modulated by SH-specific enhancers, identifying , , and as the core hub genes. Collectively, this study provides a robust data resource, identifying candidate genes and regulatory elements associated with crossbreeding-related muscle phenotypes. - Source: PubMed
Publication date: 2026/04/04
Cheng JiangboXu DanTian HuibinZhang XiaoxueZhao LimingZhang RunanWang JianlinXiao JinyuLi FadiWang WeiminZhang Deyin - This study aimed to elucidate chemerin's role in gestational diabetes mellitus (GDM)-related fetal endothelial dysfunction and its association with non-invasive hemodynamic parameters. - Source: PubMed
Zeng ShilinWang HongyingYang WanyingZeng YuzhouShenTu WeihuiFang Yi - Chemerin (RARRES2) is a multifunctional adipokine widely implicated in metabolic, inflammatory, cardiovascular, and neoplastic diseases, yet its clinical interpretation remains confounded by reliance on "total chemerin" measurements that obscure its proteoform-specific signaling. This single value is mechanistically misleading because chemerin is secreted as an inactive precursor and undergoes extracellular proteolytic processing into C-terminal isoforms with graded receptor potency and compartment-specific distribution. This review decodes chemerin's functional duality through three integrated layers: (1) protease-encoded isoform "barcodes" that dictate bioactivity, (2) compartment-specific isoform landscapes in human biofluids and disease microenvironments, and (3) receptor context across CMKLR1, GPR1, and CCRL2 that shapes signaling output. We provide a conceptual roadmap for translating chemerin biology, emphasizing isoform-resolved quantification via targeted /MRM-MS and a compartment-aware framework for interpreting clinical associations. This framework helps interpret heterogeneous disease associations and highlights testable entry points for context-specific targeting. - Source: PubMed
Publication date: 2026/03/06
Wang JingDeng JiangmingXiao TingMeng Wen