Rabbit Anti-Human CLIC4
- Known as:
- Rabbit Antibody toHuman CLIC4
- Catalog number:
- 129-10207
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CLIC4
Related genes to: Rabbit Anti-Human CLIC4
- Gene:
- CLIC4 NIH gene
- Name:
- chloride intracellular channel 4
- Previous symbol:
- -
- Synonyms:
- DKFZP566G223, CLIC4L, P64H1, H1, huH1, p64H1
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-31
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Anti-Human CLIC4
Related articles to: Rabbit Anti-Human CLIC4
- The yellowfin seabream (Acanthopagrus latus) is a significant economic fish along the southeast coast of China. Recently, the drastic decline in the wild populations, exacerbated by overfishing and climate change, has heightened our reliance on aquaculture. However, the current lack of research on its domestication hinders effective conservation of wild populations and balanced management alongside the aquaculture industry. Studies on body characteristics have shown that wild yellowfin seabream possess a higher body, while cultured ones exhibit a wider body. Whole-genome SNP analysis revealed moderate genetic differentiation between cultured and wild populations. Further analyses of linkage disequilibrium, heterozygosity, and genetic diversity revealed that the degree of SNP linkage was lower in the wild population compared to the cultured population. In contrast, heterozygosity and nucleotide polymorphisms were significantly higher in the wild population (P < 0.001 and P < 0.05, respectively). Additionally, over 300 candidate genes were identified in each cultured population through genomic selection signature analysis, with 67 key genes shared among all three, which were linked to growth and development (ghrb, ghsra, and cfl1), immune response (aire, cd36, and igbp1), and salinity adaptation (abcc3, clic4, and kcnk15). Enrichment analysis indicated that the key candidate genes were significantly enriched in pathways related to protein kinase activity, ion binding and growth hormone synthesis, secretion and action (FDR < 0.05). The findings provide valuable insights into the variation in body size of yellowfin seabream under domestication selection and offer an important theoretical basis for the genetic improvement of yellowfin seabream. - Source: PubMed
Publication date: 2026/08/13
Gao ZhanyuanWang WenhaoLiang XuanguangHuang JunrouHu YanFeng JianxiangLu Jianguo - - Source: PubMed
Publication date: 2026/08/04
Chen RuiPan ChiMao XinyuZhang YantongChen GangXu MengtingNivar JohnTao YuanxiangCao HongJunLi - In addition to its involvement in maintaining membrane electrical balance, ion homeostasis, and transmembrane transport, intracellular chloride channel protein 4 (CLIC4) is regulated by signaling molecules such as TGF-β, P53, Myc, and TNFα and is closely associated with apoptosis. Nevertheless, the expression patterns and functional roles of CLIC4 across different cancer types remain inconsistent and are not fully understood. In this study, we initially observed reduced CLIC4 expression in non-small cell lung cancer (NSCLC) through bioinformatics analysis and further validated this downregulation using multidimensional experimental approaches. We established stable NSCLC cell lines with CLIC4 overexpression or knockdown to investigate its effects on cellular proliferation, migration, and invasion. Subsequent RNA sequencing of CLIC4-overexpressing cells revealed that CLIC4 suppressed MAPK-related signaling pathways, which was confirmed by western blotting. These findings suggest that CLIC4 may inhibit the progression of NSCLC by downregulating MAPK signaling, offering potential insights for novel diagnostic and therapeutic strategies in NSCLC. - Source: PubMed
Publication date: 2026/07/21
Gao PengxiangLu WanjunTan XinyuZhang WeiXu Xinping - Cervical cancer (CC) ranks among the most prevalent malignant neoplasms affecting women worldwide. Tumor recurrence, distant metastases, and chemotherapy resistance significantly hinder long-term clinical survival and therapeutic outcomes. Clinical studies indicate a heightened prevalence of depressive symptoms and major depressive disorder (MDD) among CC patients, suggesting the possibility of bidirectional adverse biological interactions between cervical tumor progression and depressive states. However, the shared molecular signatures underlying both cervical carcinoma and depressive disorders have yet to be fully elucidated, highlighting the need for identifying reliable molecular markers for supplementary diagnosis and prognostic stratification of CC. - Source: PubMed
Publication date: 2026/07/20
Zhang Hua-HuaLiu MinChen Ya-NiZhang Ming-RuZhang JingHe Jing - Membrane channels are central to bladder function, yet current understanding is shaped disproportionately by a few well-studied families such as TRPA1 and TRPV1. To provide a more balanced view, this review analyzed emerging human transcriptomic datasets to identify the channels most highly expressed in the urinary bladder and examined how they remodel in bladder outlet obstruction and denervation. Sixty-seven channels were prominently expressed at the mRNA level in GTEx bladder tissue, with correlation analyses and protein expression data assigning many to smooth muscle, urothelial, endothelial, or neuronal compartments. Several abundant channels remain largely unstudied in urological contexts, including , , and . Disease-associated remodeling revealed shared and model-specific patterns. Outlet obstruction produced marked upregulation of L-type Ca channel auxiliary subunits and robust changes in CLIC-family channels, whereas denervation induced broader channel downregulation not explained by nerve loss alone. Three channels, , and , were concordantly altered in both conditions, suggesting coordinated changes within interstitial cell networks and mechanotransductive pathways. These findings highlight a diverse and incompletely explored bladder "channel-ome." Expanding research beyond traditional targets may uncover new mechanisms underlying storage and voiding dysfunction and provide opportunities for therapeutic innovation in lower urinary tract disease. - Source: PubMed
Publication date: 2026/04/07
Swärd KarlAndersson Karl-ErikUvelius Bengt