ATG9B Antibody Autophagy Antibody
- Known as:
- ATG9B Antibody Autophagy Antibody
- Catalog number:
- AUT-5797
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ATG9B Antibody Autophagy
Ask about this productRelated genes to: ATG9B Antibody Autophagy Antibody
- Gene:
- ATG9B NIH gene
- Name:
- autophagy related 9B
- Previous symbol:
- NOS3AS
- Synonyms:
- FLJ14885, APG9L2, SONE
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-24
- Date modifiied:
- 2016-10-05
Related products to: ATG9B Antibody Autophagy Antibody
Related articles to: ATG9B Antibody Autophagy Antibody
- Coronary artery disease (CAD) is a leading cause of death and disability worldwide. Although genome-wide association studies (GWAS) have identified over 300 loci associated with CAD risk, the molecular mechanisms linking these variants to disease and subclinical atherosclerosis are not fully understood. - Source: PubMed
Publication date: 2026/08/03
Yang ChaojieAguet FrancoisAuguste GaelleArdlie KristinGerszten RobertPost Wendy SWheeler Heather ETaylor Kent DKasela SilvaLappalainen TuuliIm Hae KyungDurda PeterJohnson CraigGuo XiuqingLiu YongmeiPolak JosephHerrington DavidClish ClaryVan Den Berg DavidTracy Russell PCornell ElaineBlackwell TomPapanicolaou GeorgeVargas Jose DBekiranov StefanMcNamara Coleen AMiller Clint LRotter Jerome IRich Stephen SManichaikul Ani - Sepsis-associated encephalopathy (SAE) is a severe complication with high mortality and limited therapeutic options. Molecular hydrogen (H₂) has shown neuroprotective potential, but its mechanism remains elusive. - Source: PubMed
Publication date: 2026/07/10
Yu XiaoliHuang XiaofanSong YuLiu JianfengHuang FeiCui JiatianXie KeliangCui Yan - : Autophagy is an evolutionarily conserved intracellular degradation mechanism that is regulated by a set of autophagy-related (ATG) proteins. The only transmembrane protein among ATGs is the lipid scramblase ATG9, which exists in the form of two paralogs, ATG9A and ATG9B, in humans and other vertebrates. : Here, we analyzed human and murine skin transcriptome and proteome datasets for the expression of ATG9 paralogs and performed comparative genomics to determine their conservation during the evolution of amniotes (mammals and sauropsids). : The expression of , but not of , is enriched in differentiated epidermal keratinocytes and in skin appendages of humans and mice. In contrast to the conservation of in all major clades of amniotes, has been lost in at least three phylogenetic lineages. Cetaceans, which have unique skin adaptations to aquatic life, harbor mutations that disrupt the open reading frame of . Many or all species of turtles () and crocodilians () have entirely lost the gene. : has undergone independent pseudogenization or gene loss in different subgroups of amniotes. In mammalian species that have retained the gene, its expression pattern indicates functions of in the skin and skin appendages. - Source: PubMed
Publication date: 2026/06/09
Sukseree SupawadeeEckhart Leopold - Autophagy is a highly conserved eukaryotic cellular process whose dysfunction results in human pathologies including cancer and neurodegenerative disease. First identified in yeast, genes are central players in autophagy. Mutations in core autophagy genes and have been previously reported to cause rare genetic disorders with autosomal recessive inheritance. - Source: PubMed
Publication date: 2026/06/05
Kılıç SevalEsmen KeremMéreaux Jean-LoupOto Ayşe MirayKose Tansu BilgeSever-Bahcekapili MelikeEren-Koçak EmineDemir ŞeydaHız A SemraAfzal ErumFiroozfar ZahraKarakülah GökhanBagriyanik H AlperGuillot-Noel LénaCoarelli GiuliaHoulden HenryEfthymiou StephanieDurr AlexandraÖztürk MehmetDiril M Kasim - Alopecia areata (AA) is a common autoimmune alopecia disease. Evidence suggests that autophagy-related genes (ARGs) may contribute to its pathophysiology. This study aims to explore and identify potential autophagy-related biomarkers and molecular subtypes in AA. In this study, autophagy-related differential expression genes (ARDEGs) in AA were identified by comparing the differentially expressed genes (DEGs) in the GSE68801 dataset with the ARGs. Then, we applied three different machine learning methods to identify key hub genes and further verified them on independent datasets. We used the receiver operating characteristic (ROC) curve to evaluate the diagnostic potential of these hub genes and constructed a predictive nomogram. In addition, this study also used the consensus clustering method to define two AA subtypes and explored their immune characteristics and functional pathways through ssGSEA, MCPcounter and enrichment analysis. Experimental validation included qRT-PCR for four hub genes and Western blotting for critical autophagy markers. Our analysis detected 10 ARDEGs in AA. Applying three machine learning algorithms, we identified four candidate hub genes, , , and , and verified their expression patterns in independent cohorts. The combined four-gene model and nomogram showed potential diagnostic performance. Consensus cluster analysis divided AA cases into two subtypes, each associated with different immune infiltration and functional pathways. Downregulation of and and upregulation of were verified by qRT-PCR. Western blotting further suggested altered autophagy-related protein expression in AA lesions, characterized by a reduced LC3B-II/I ratio and Beclin-1 expression and increased SQSTM1 expression. This study identified four candidate autophagy-related genes and two exploratory molecular subtypes in AA and may provide clues for understanding autophagy-related immune dysregulation and support further validation of candidate diagnostic markers. - Source: PubMed
Publication date: 2026/05/23
Li YufenZhang XiaolinWang JiatingJiang Yiqun