Ask about this productRelated genes to: KLHL5 Blocking Peptide
- Gene:
- KLHL5 NIH gene
- Name:
- kelch like family member 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p14
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-09
- Date modifiied:
- 2016-10-05
Related products to: KLHL5 Blocking Peptide
Related articles to: KLHL5 Blocking Peptide
- Feed efficiency (FE) and growth traits are key determinants of profitability in the chicken industry. Using genome-wide association studies (GWAS) in 432 Wenchang chickens, we identified 28 significant and 1,063 suggestive genes associated with 6 FE and growth traits. We conducted colocalization analyses between GWAS loci and cis-eQTLs and detected 4 GWAS loci with 4 unique eGenes including LAP3, PDS5A, KLHL5 and KLB. We also examined the cis-eQTL analysis results of ChickenGTEx and integrated them with the results of our GWAS, which detected two SNPs (4_75971034, 4_75971177) regulating LAP3. Moreover, two significant InDels (4_75971045, 4_75971140) are identified in the LAP3 gene using GWAS, three genotypes significantly affecting the expression levels of this gene in transcriptomic analyses of 114 liver tissues, and highly linked to two SNPs, so these InDels may also affect LAP3. Our findings reveal key genetic variants and genes, contributing to a deeper elucidation of the molecular mechanisms that drive FE and growth traits in chickens. - Source: PubMed
Publication date: 2026/05/25
Zhang YapengZhang YinLuo NaCai KeqiLiang XiaochenLan YiLiu RanranZhao Guiping - Thymic carcinoma (THYM) is a mediastinal malignant tumor that seriously endangers human health. Cancer-associated fibroblasts (CAFs) are implicated in many cancers, but their role in THYM remains unclear. Western blot and reverse transcription-quantitative polymerase chain reaction were used to analyze expression levels. Exosomes were isolated and characterized by transmission electron microscopy and nanoparticle tracking analysis, and their uptake was assessed using PKH26 labeling. Cell functions were evaluated with cell counting kit-8, colony formation, and Transwell assays, while M2 macrophages were identified by flow cytometry for CD206. Bioinformatics databases analyzed gene correlations. The interaction between signal transducer and activator of transcription 3 (STAT3) and the kelch-like family member 5 (KLHL5) promoter was confirmed by chromatin immunoprecipitation and dual-luciferase reporter assay. Xenograft models were established to verify the effects of STAT3 in tumor growth, and protein expression in tissues was assessed by immunohistochemistry. Exosomes were successfully isolated from CAFs. STAT3 was up-regulated in CAF-derived exosomes compared to those from normal fibroblasts (NFs). Knockdown of STAT3 in CAF-derived exosomes repressed THYM cell viability, colony formation, migration, and invasion, as well as M2 macrophage polarization. STAT3 expression was positively correlated with KLHL5 and bound to the KLHL5 promoter. Furthermore, KLHL5 silence inhibited THYM cell malignant behaviors and M2 macrophage polarization, whereas KLHL5 overexpression attenuated the inhibitory effects of STAT3 knockdown. Similarly, silencing STAT3 in CAF-derived exosomes blocked tumor growth in vivo. CAF-derived exosomes transfer STAT3 to THYM cells, promoting THYM malignant progression and M2 macrophage polarization by transcriptionally activating KLHL5. - Source: PubMed
Publication date: 2026/02/25
Chu JianhuLuo DongboWang YangLiu YiShalai AdiliJin ShiyingGao Yunfei - Helicobacter pylori (H. pylori) is a major risk factor for gastric cancer (GC) and multiple other chronic illnesses. Host genetic factors influence the susceptibility to H. pylori infection, as evidenced by elevated concordance in monozygotic twins and racial disparities independent of socioeconomic status. Leveraging meta-analyses and in silico functional annotation, we investigated host genetic susceptibility to H. pylori infection, and to examine how these variants may influence gastric cancer (GC) risk. - Source: PubMed
Zhao Wen-JingXu Heng-MinZhang ChaoJiang Xiao-WenPan Kai-FengLi Wen-Qing - Alzheimer's disease (AD) is a leading cause of dementia characterized by neuroinflammation and immune dysregulation. Perivascular macrophages (PVMs) play a crucial role in the onset and progression of AD, yet the specific molecular mechanisms remain understudied. This study explored the molecular mechanisms of PVMs in AD using single-cell sequencing combined with Mendelian randomization (MR) analysis. We analyzed data from GSE264648 and eQTLGen and identified four key genes that were significantly associated with AD risk: IFNGR1, KLHL5, NUMB, and WDFY4. Functional annotation revealed that PVMs were involved in immune regulation and metabolic pathways, particularly IL-6_JAK_STAT3 and Notch signaling. Immune infiltration analysis showed increased M2 macrophages in AD patients, suggesting their roles in neuroinflammation. Pseudo-time analysis highlighted developmental shifts in PVMs during disease progression. Our findings offer novel insights into the role of PVMs in AD and provide a foundation for future research on modulating neuroinflammation and slowing AD progression through PVM-targeted interventions. - Source: PubMed
Publication date: 2025/07/07
Zhang MinLiu ShufangZhao YananWu PingTian ShouyuanWu ZhifangLi Sijin - Kelch-like protein 5 (KLHL5) is highly expressed in colorectal cancer (CRC) compared to that in adjacent normal mucosa, and its expression level increases with CRC stage, showing a correlation with poor prognostic factors. However, its functional role in the malignant progression still remains unknown. To elucidate the role of KLHL5 in CRC, we characterized human CRC cell lines, including HCT116 and SW480, under KLHL5-depleted conditions. KLHL5-depleted HCT116 and SW480 cells suppressed their growth and migration in culture. Further duration induced cell death characterized by apoptotic cell death with down-regulation of antiapoptotic factor Bcl-2 and up-regulation of proapoptotic factors Bac, Boc, Puma, Bid, Noxa, and Bik. Proteomic analyses indicated KLHL5 depletion suppressed cell cycle progression by affecting multiple pathways, including the activation of the G2/M DNA damage pathway and inhibition of the G1/S transition. Further biochemical and cell biological analyses revealed the downregulation of CDT1 and CDC6 proteins, which are essential factors for the initiation of DNA replication, and the downregulation of cyclins A and B, which are essential factors for the progression of S and G2/M phases. Arrested cells undergo apoptotic cell death. Taken together, these data strongly indicate that KLHL5 expression in CRC serves as a survival factor to strengthen the cell cycle and protect against apoptotic cell death under harsh tumor microenvironments. - Source: PubMed
Publication date: 2025/07/01
Habu KyosukeMatsuoka YosukeHiyoshi HiromiNakayama JunWatanabe KatsuyaTate SotaSakaue TomohisaMurai JunkoUno KonomuNishie HirotadaKubota EijiKataoka HiromiJoh TakashiWatanabe YujiOshikiri TaroHigashiyama Shigeki