KLHL8 antibody
- Known as:
- KLHL8 (anti-)
- Catalog number:
- orb101608
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- KLHL8 antibody
Related genes to: KLHL8 antibody
- Gene:
- KLHL8 NIH gene
- Name:
- kelch like family member 8
- Previous symbol:
- -
- Synonyms:
- KIAA1378
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-10
- Date modifiied:
- 2016-10-05
Related products to: KLHL8 antibody
Related articles to: KLHL8 antibody
- Hepatocellular carcinoma (HCC) remains a global health challenge with a high recurrence rate, highlighting the need to decipher its underlying molecular mechanisms. While circular RNAs (circRNAs) are known to regulate gene expression, the landscape of competitive splicing-the dynamic balance between back-splicing and linear splicing-during HCC initiation and recurrence remains largely unexplored. Leveraging rRNA-zero RNA-seq data from GSE169289 (comprising 34 primary, recurrent, and non-recurrent HCC samples with paired controls), this study utilized an upgraded SUVA pipeline to systematically profile circRNA-associated alternative splicing events. By integrating four distinct algorithms, we identified 9,652 high-confidence circRNAs. Our analysis revealed extensive differential splicing events distinguishing tumor from normal tissues, and notably, recurrent from non-recurrent tumors, with host genes enriched in chromatin remodeling and ubiquitin-dependent pathways. Specifically, we observed a conserved attenuation in the competitive splicing of the LARP1B circRNA in tumor tissues, which correlated with host gene downregulation and poor prognosis. In the context of recurrence, circ-KLHL8 exhibited specific splicing suppression; in silico modeling suggests a potential mechanism where circ-KLHL8 loss relieves the sponging of miRNAs, thereby suppressing the tumor suppressor GLYCTK. Furthermore, RBP-circRNA co-regulatory network analysis implicated HNRNPU and CPSF4 as potential upstream regulators of initiation-related splicing, and DKC1 as a modulator of recurrence-associated events. Collectively, this study provides the first systematic characterization of the competitive splicing landscape in HCC, proposing a novel theoretical framework and candidate targets for diagnostic and therapeutic interrogation. - Source: PubMed
Publication date: 2026/05/14
Jiang SunluCui NingNie LeiShen JianZhu XianminLi Hong - Ferroptosis, characterized by iron-dependent lipid peroxidation, is considered a key cell death pathway activated during ischemic stroke. GPX4, a negative regulator of ferroptosis, exacerbates brain damage. However, the precise regulatory mechanisms governing this process remain poorly understood. Here, we determined that oxygen-glucose deprivation/reoxygenation (OGD/R)-induced GPX4 degradation is primarily dependent on autophagy activation. Mechanistically, the E3 ubiquitin ligase KLHL8 tags GPX4 through ubiquitination and promotes its binding to the selective autophagy receptor TAX1BP1, thereby synergistically mediating GPX4's autophagic-lysosomal degradation. Clinical database analysis also confirmed that KLHL8 and TAX1BP1 expression are significantly upregulated in brain tissue from patients with ischemic stroke and positively correlated with ferroptosis scores. Therapeutic approaches have shown that AAV-mediated GPX4 overexpression or the use of autophagy inhibitors can effectively stabilize GPX4 levels, inhibit neuronal ferroptosis, and significantly improve cerebral infarction and neurological function in mice undergoing middle cerebral artery occlusion (MCAO). In particular, the combination of GPX4 overexpression and artesunate demonstrated a potent synergistic neuroprotective effect. These findings suggest that a cascade consisting of KLHL8-mediated ubiquitination and TAX1BP1-mediated selective autophagy is a key pathway for GPX4 degradation, and that the KLHL8-TAX1BP1-GPX4 regulatory axis provides a potential therapeutic target for ischemic stroke. - Source: PubMed
Publication date: 2025/12/30
Zhao JingjingLiu YanfeiSun WenhuaLi WeiweiXu Zheng - Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer-related mortality worldwide. Mendelian randomization (MR) has emerged as a powerful approach for therapeutic target identification in HCC. In this study, we applied two-sample MR to assess the causal effects of multiple genes on HCC risk. Replication analyses integrated summary-data-based MR, Bayesian co-localization, and protein-protein interaction networks with druggability assessment to prioritize targets. Single-cell RNA sequencing validated cell-type-specific expression patterns in T cells, endothelial cells, and hepatocytes. MR-, summary-data-based MR-, and co-localization-based approaches identified target genes associated with HCC risk, comprising 3 first-level targets (HLA-DPA1, MBTPS1, and TIMP3), 2 second-level targets (TNXB and HSD17B11), and also 4 tertiary targets (HLA-DPB1, PLD2, KLHL8, and TGFBR1). All in all, this research identifies several potential therapeutic targets relevant to the risk of HCC and provides new insights into the identification of therapeutic agents for the treatment of HCC. - Source: PubMed
Tang ChaoZhu ShuangjingDing Zhen - Maternal protein homeostasis and timely degradation of maternal mRNAs are essential for meiotic cell-cycle progression and subsequent embryonic development, but the mechanisms of maternal protein degradation are poorly understood. Here, we show that KLHL8, a substrate adaptor of Cullin-RING E3 ubiquitin ligases, is highly expressed in mouse oocytes and co-localizes with mitochondria. Oocyte-specific deletion of Klhl8 causes oocyte maturation defects and female infertility. ZAR1, an RNA binding protein that is required for mitochondria-associated ribonucleoprotein domain (MARDO) dissolution, is specifically recognized and degraded by KLHL8-mediated ubiquitination. In Klhl8-deficient oocytes, ZAR1 accumulation causes abnormal MARDO and mitochondria clustering, correlating with impaired maternal mRNA decay. Supplementation with exogenous Klhl8 mRNA rescues the degradation of ZAR1 and the dissolution of the MARDO in Klhl8 oocytes. Taken together, our study shows that KLHL8 mediates the ubiquitination and degradation of ZAR1, thus regulating maternal mRNA clearance during oocyte maturation. These findings provide new insights into the roles of the ubiquitin proteasome system during oocyte maturation and establish an interaction network between ubiquitination modification, RNA binding proteins, and maternal mRNA. - Source: PubMed
Publication date: 2025/07/28
Fan HuizhenLiu RuyiYu RanChen BiaobangLi QiaoliMu JianWang WeijieWu TianyuHe LinWang LeiSang QingZhang Zhihua - During mammalian spermatogenesis, the cytoskeleton system plays a significant role in morphological changes. Male infertility such as non-obstructive azoospermia (NOA) might be explained by studies of the cytoskeletal system during spermatogenesis. - Source: PubMed
Publication date: 2025/01/25
Hashemi Karoii DanialAzizi HosseinDarvari MaryamQorbanee AliHawezy Dawan Jamal