ATG4C
- Known as:
- ATG4C
- Catalog number:
- 002138A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATG4C
Related genes to: ATG4C
- Gene:
- ATG4C NIH gene
- Name:
- autophagy related 4C cysteine peptidase
- Previous symbol:
- AUTL1, APG4C
- Synonyms:
- FLJ14867, AUTL3
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-13
- Date modifiied:
- 2016-02-23
Related products to: ATG4C
Related articles to: ATG4C
- Genome-wide association studies (GWAS) have uncovered multiple loci associated with atopic dermatitis (AD), although mechanistic understanding remains limited. Here, we examine a risk variant in the aquaporin 3 (AQP3) promoter and propose a mechanistic link between genotype to altered autophagy, skin barrier integrity, and wound healing in AD. A GWAS involving 1261 AD cases and 4062 controls of Chinese ancestry from the Singapore-Malaysia cohort was performed. Linkage disequilibrium (LD) analysis and cis-eQTL datasets were used to assess regulatory associations. Functional effects of promoter variants were validated using in vitro luciferase assays and ex vivo transcriptomic profiling. In vitro experiments in HaCaT keratinocytes investigated the effect of siRNA-mediated AQP3 knockdown on autophagy, skin barrier integrity, and wound closure. A discovery GWAS identified significant association between AD and SNP rs12555686 (p = 1.67 × 10, OR = 1.89), located in the promoter of AQP3. Two additional SNPs in strong LD (rs2231225, rs3758279) formed a major haplotype associated with reduced AQP3 expression. Reduced AQP3 expression was associated with decreased autophagy markers (Beclin1, ATG5, ATG12, GABARAPL2, LAMP2, ATG4C), increased senescence markers (p21, GADD45A, SERPINE1), and elevated inflammatory cytokines (IL8, IL1B, TNF). Lastly, AQP3 knockdown in HaCaT keratinocytes reduced steady-state LC3B-II/LC3B-I ratio, reduced occludin expression, and delayed wound healing in vitro. Promoter variants in AQP3 link genetic susceptibility to gene signatures consistent with altered autophagy, cellular senescence, and inflammation in AD. These findings highlight AQP3 as a potential modulator of both epithelial and immune-related mechanisms in AD pathogenesis. - Source: PubMed
Lim Yi Ying ElizaSio Yang YieLam Terence Yin WengSay Yee-HowReginald KavitaChew Fook Tim - Eggshell quality is a critical trait in poultry production, as it directly influences economic outcomes. The genetic architecture underlying this trait remains poorly characterized. In this study, we conducted a genome-wide association study (GWAS) on Chinese Wenshang Barred chickens at 43 weeks of age to identify genomic loci and candidate genes associated with eggshell quality. This analysis revealed 87 significant SNPs and 14 candidate genes. Genes including , , , , and were associated with eggshell weight; , , , , and with eggshell thickness; and and with eggshell strength. Notably, three SNPs emerged as the most promising markers for eggshell quality, though their functional roles in laying hens require further investigation. This study advances our understanding of the genetic basis of eggshell quality and holds significant practical implications for improving this trait through targeted breeding strategies. - Source: PubMed
Publication date: 2026/07/11
Wang JieHan HaixiaLiu JieLei QiuxiaLiu WeiSun YanHao DanLi FuweiWang XinxiaCao DingguoZhao XinhuaZhou Yan - Metabolic dysfunction-associated steatotic liver disease (MASLD) is a globally prevalent chronic liver disorder for which effective therapeutic options are scarce. Autophagy is pivotal in sustaining hepatic lipid homeostasis, and cytoskeletal proteins modulate autophagic flux. However, the role of myosin heavy chain 11 (MYH11) in the pathogenesis of MASLD remains elusive. Bioinformatic mining of Gene Expression Omnibus (GEO) datasets identified MYH11 as a key autophagy-associated differentially expressed gene that exhibited robust diagnostic performance in MASLD. MYH11 expression was markedly downregulated in the livers of db/db mice and in the serum of patients with MASLD, and this reduction was negatively correlated with peripheral levels of alanine transaminase (ALT), total cholesterol (TC), triglycerides (TG), and LDL-C. Gain- and loss-of-function experiments validated MYH11's protective role : AAV8-mediated MYH11 overexpression mitigated hepatic steatosis, inflammation, and fibrosis in db/db mice and inhibited extracellular matrix (ECM) deposition in palmitic acid-challenged LX-2 cells and inflammatory responses in palmitic acid-challenged HepG2 cells, whereas MYH11 silencing exacerbated these pathological changes. Mechanistically, MYH11 boosts autophagic flux by upregulating ATG4A expression, and MYC directly interacts with the MYH11 promoter to regulate its transcriptional activity. In summary, MYH11 functions as a MYC-regulated protective factor in MASLD, alleviating hepatic damage via the MYH11-ATG4A-autophagy axis. Thus, it holds promise as a candidate diagnostic biomarker and prospective therapeutic target for MASLD. - Source: PubMed
Publication date: 2026/07/21
Liu Guang-PengMa Xiao-HanWang Hong-QianTong Cheng-ChengChen Xi - Osteosarcoma is one of the most prevalent malignant tumors in pediatric cancer, with survival rates remaining stagnant for over a decade, particularly among patients with metastatic disease. Thus, identifying novel therapeutic targets is critical for improving clinical outcomes. The ATG4 family (ATG4A, ATG4B, ATG4C, and ATG4D) encodes proteases essential for autophagy, a process implicated in cancer progression and drug resistance. However, the role of ATG4 proteins in osteosarcoma remains unclear. This study showed that silencing ATG4 family members using small interfering RNA (siRNA) induced G1-phase cell cycle arrest and promoted cell death in osteosarcoma cells. Among them, ATG4D knockdown significantly impaired cell migration and invasion. Consistently, stable knockdown of ATG4D via short hairpin RNA (shRNA) reduced cell motility and tumorsphere formation. Moreover, ATG4D depletion enhanced autophagic markers, including LC3B-II puncta and p62 protein levels, and sensitized osteosarcoma cells to starvation and chemotherapy-induced cell death. In vivo, osteosarcoma cells harboring ATG4D-targeting shRNA exhibited reduced tumor growth and elevated apoptosis in xenografted mice compared to control cells. Clinically, ATG4D protein expression was elevated in osteosarcoma tissues compared to normal bone cells, with higher levels correlating with poor overall survival, particularly in patients older than 10 years or with tumors located in the lower limbs. These findings suggest that ATG4D may serve as a potential diagnostic biomarker and therapeutic target for osteosarcoma. - Source: PubMed
Liu Pei-FengYang Shan-WeiYang Wen-HsinHuang Shu-FangTsai Ching-YangHsu Chien-JenTseng Ho-HsingLee Cheng-HsinShu Chih-Wen - While components of the autophagy pathway have been linked to cancer prognosis, their relationship with clinical outcomes remains unclear. This study investigates the expression levels of autophagy-related genes (ATGs) at both mRNA and protein levels in nasopharyngeal carcinoma (NPC) and their association with Epstein-Barr virus (EBV) infection, clinicopathological characteristics, and clinical outcomes. - Source: PubMed
Publication date: 2025/06/24
Alanazi Abdullah EAwadalla MaaweyaAlowaini AmaniAlamri SaadAlGhamdi Doaa AliAbdel Halim Alyaa SAli Mohamed A MAlosaimi Bandar