Anti_Human, mab CXCL6 Source Mouse
- Known as:
- Anti_Human, mab CXCL6 Source Mouse
- Catalog number:
- 101-M356
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CXCL6 Source Mouse
Related genes to: Anti_Human, mab CXCL6 Source Mouse
- Gene:
- CXCL6 NIH gene
- Name:
- C-X-C motif chemokine ligand 6
- Previous symbol:
- SCYB6
- Synonyms:
- GCP-2, CKA-3
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-03-01
Related products to: Anti_Human, mab CXCL6 Source Mouse
Related articles to: Anti_Human, mab CXCL6 Source Mouse
- S100A12 as an indispensable molecular components inflammatory cytokines in human physiology. Notably, similar pathological mechanisms involving chronic low-grade inflammation are also observed in intervertebral disc degeneration (IVDD) and osteoporosis (OP), making the interplay between these diseases and inflammatory cytokines indisputable. Nevertheless, the precise identity of cytokines that concurrently fuel IVDD and OP remains elusive, hindering targeted therapeutic strategies. - Source: PubMed
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Wang ZexinChen BinLiu ZhenchuanZhang YuanqiangHan Leixiang - The N6-methyladenosine (mA) reader YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) plays a critical role in the tumorigenesis of intrahepatic cholangiocarcinoma (ICC), but its function in the tumor immune microenvironment remains unclear. RNA sequencing analysis of human ICC samples revealed that, among mA-related regulators, YTHDF1 exhibited the most significant negative correlation with immune score. In multiple ICC mouse models, Ythdf1 overexpression enhanced the recruitment of myeloid-derived suppressor cells (MDSCs) and suppressed cytotoxic CD8 T cell responses, promoting ICC progression. Immunostaining of human ICC tissue microarray verified that high YTHDF1 protein expression was significantly associated with increased accumulation of MDSCs and decreased infiltration of CD8 T cells. Mechanistically, YTHDF1 bound to the mA site of FOSL2 mRNA and promoted the translation of FOSL2, a transcription factor driving cytokine CXCL6 expression. Consequently, elevated CXCL6 recruited and activated MDSCs by binding to its receptor CXCR2, leading to the dysfunction of CD8 T cells in ICCs. In addition, targeting YTHDF1 alongside blockade of its downstream chemokine pathway enhanced the efficacy of anti-PD-L1 treatment in preclinical ICC mouse models, serving a promising strategy for improving immunotherapy efficacy in ICC. - Source: PubMed
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