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
- - 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 - In recent years, great interest has been committed to the search for alternative clinical treatments for herpetic infections that reduce side effects, overcome drug resistance, and combat the intense inflammatory response triggered by viral infection. Pistachios () are known to contain polyphenols, pharmacologically active compounds with both immunomodulatory and antiviral activities. The present work investigates the antiviral properties of pistachio extracts against HSV-1 and their potential immunomodulatory effect on human monocytic cells, with a focus on NF-κB signaling. The RT2 Profiler PCR array was used to identify differential expression of chemokines during infection and pretreatment. We discovered that HSV-1 induces potent cytokine and chemokine activation in monocytes, and that this activation is significantly reduced by in vitro treatment with pistachio extracts. Our focus included CXCL10, CXCL11, CCL13, CCL2, CCL4, CCL13 and the receptor CMKLR1, which were particularly expressed after HSV-1 replication and downregulated by pretreatment with pistachio extracts. We further confirmed this inhibitory activity using zeaxanthin, a bioactive carotenoid found in pistachios, which has previously shown to inhibit HSV-1 replication in permissive cells. In addition, by blocking viral replication with phosphonoacetic acid (PAA), we demonstrated that in HSV-1-infected THP-1 cells, activation of CXCL10, CXCL11, CCL13, CCL2, CCL4, CCL13 and CMKLR1 was significantly downregulated, suggesting that chemokine activation is partially dependent on active HSV-1 replication. Lastly, using THP-1-dnIκBα cells, we have demonstrated that chemokine accumulation was correlated with HSV-1-induced NF-κB activation. Importantly, when neuronal (SH-SY5Y) and epithelial (HEp-2) cells were exposed to supernatants derived from pistachio extracts and zeaxanthin-treated infected THP-1 cells, we observed a significant reduction in the production of new HSV-1 viral progeny compared to the untreated infected THP-1 cells. In conclusion, the study highlights the use of pistachio extracts and zeaxanthin as a promising therapeutic approach against HSV-1. Notably, it offers valuable insights into the complex virus-host interaction, demonstrating how HSV-1 modulates the chemokine-mediated cell response, including CXCL10, CXCL11, CCL13, CCL2, and CCL4, and the receptor CMKLR1, to maintain a delicate balance with the host cell, thereby promoting viral persistence. - Source: PubMed
Publication date: 2026/03/28
Pennisi RosamariaCosta MariannaTamburello Maria PiaTrischitta PaolaMandalari GiuseppinaSciortino Maria Teresa