Polyclonal Rabbit ATG16L2 Antibody
- Known as:
- Polyclonal Rabbit ATG16L2 Antibody
- Catalog number:
- KA0322
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ATG16L2 Antibody
Related genes to: Polyclonal Rabbit ATG16L2 Antibody
- Gene:
- ATG16L2 NIH gene
- Name:
- autophagy related 16 like 2
- Previous symbol:
- -
- Synonyms:
- FLJ00012, WDR80, ATG16B
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-13
- Date modifiied:
- 2015-11-24
Related products to: Polyclonal Rabbit ATG16L2 Antibody
Related articles to: Polyclonal Rabbit ATG16L2 Antibody
- Autophagy, a fundamental cellular process, is indispensable for maintaining cellular homeostasis through the regulated degradation and recycling of intracellular components, including damaged organelles and invading pathogens. ATG16L2 is a key autophagy gene essential for autophagosome formation and maturation. Unraveling the intricate transcriptional regulation of such autophagy-related genes is paramount for optimizing livestock germplasm and enhancing breeding programs. This study aimed to comprehensively elucidate the transcriptional regulation of the goat ATG16L2 gene. Tissue-specific qPCR analysis revealed the highest ATG16L2 mRNA expression in the goat spleen among key tissues examined (liver, spleen, lung, kidney, fat, rumen, and small intestine). Subsequently, to characterize the ATG16L2 promoter, we cloned a 1,304 bp upstream sequence (from -1,080 to +224 relative to the transcription start site, TSS). Truncated promoter constructs derived from this fragment were evaluated via dual-luciferase reporter assays to identify the core promoter region. To investigate the transcriptional regulation of goat ATG16L2, small interfering RNAs (siRNA) were used to target specific transcription factors. Dual-luciferase reporter assays demonstrated that deleting the identified SMAD5 binding site significantly diminished promoter activity. This was further supported by siRNA-mediated knockdown of SMAD5, which led to reduced luciferase activity in transfected goat primary fibroblasts. In conclusion, we identified the core promoter region of the goat ATG16L2 gene that maintains basal transcription and demonstrated the role of SMAD5 in its transcriptional regulation, laying the foundation for future studies on the function of goat ATG16L2. - Source: PubMed
Wang HuanZhang MengqiQian HejieChen TaoyuMeng YongLi ShiyuanNiu ShihuaMan ChurigaGao HongyanChen QiaolingDu LiWang FengyangChen Si - Systemic lupus erythematosus (SLE) and inflammatory bowel disease (IBD) are both categorized as autoimmune disorders and have similar non-specific gastrointestinal symptoms. SLE and IBD have shown shared genetic architecture in European ancestry; however, given the ancestry-specificity of genetic architecture, the shared genetic structure in East Asian ancestry remains unclear. This study reveals significant global and local genetic overlap between SLE and IBD subtypes in East Asian ancestry by using genetic correlation analyses. Cross-trait and colocalization analyses identify 64 shared loci and 19 causal variant credible sets between SLE and IBD subtypes. Notably, pleiotropic genes (HIC2, UBE2L3, ARAP1, ATG16L2, ANKS1A, and TULP1) were validated through Gene Expression Omnibus databases and previous studies. The major histocompatibility complex region emerges as a critical hub for shared genetic correlations and pleiotropic effects in SLE-IBD pathogenesis. Gene-level enrichment analyses implicate chemokine and lipid binding as underlying shared biological mechanisms. - Source: PubMed
Mo XiaoxiaoMo HuiWang ChaoPu QiuyiSha LanlanZhao LetianZhang ZhengdongWang TingWu Dongmei - The development of resistance to trastuzumab in HER2-positive breast cancer is a serious clinical problem that limits the effectiveness of targeted therapy. In a significant proportion of patients, the mechanisms in the development of resistance remain poorly understood. The BT-474 cell line was selected as an optimal model for study because it represents a HER2-positive luminal B subtype breast cancer cell line. To identify the molecular mechanisms of resistance, a comprehensive transcriptomic analysis based on RNA-seq data comparison of three independent datasets including both sensitive and trastuzumab-resistant variants was applied. The methodological approach included multistep bioinformatics analysis followed by identification of regulatory interactions. The study identified genes with increased expression (FUCA2, HSPE1, SHLD1, NMD3) and genes with decreased expression (GPC5, FSTL1, ATG16L2, POLD2) in resistant cells. Key transcription factors (E2F1, MYC, YBX1, HEY1, NFIC, TFAP2A, AP-1/JUN, NCOA1) regulating the expression of the detected genes during the development of resistance were identified. The changes identified indicate a complex reprogramming of transcriptional activity affecting cell cycle processes, DNA repair, metabolism, and the epithelial-mesenchymal transition. The findings expand our understanding of the molecular mechanisms of trastuzumab resistance and open prospects for the development of novel therapeutic strategies to overcome drug resistance in HER2-positive breast cancer. - Source: PubMed
Shifon S AKarpets I OChesnokova A SKaritskaya P EUkladov E OEvgenov I VSidorov S VGulyaeva L F - Sarcoidosis is characterized by the proliferation of noncaseating granulomas and presents as a complex chronic inflammatory disease. Autophagy plays a crucial role in the initiation, progression, and treatment resistance of various cancers. Despite the recognized importance of autophagy, the involvement of autophagy-related genes (ARGs) in the pathophysiology of ocular sarcoidosis (OS) remains largely unexplored. - Source: PubMed
Publication date: 2025/08/05
Wu ZixuanLong XiTan KangYao XiaoleiPeng Qinghua - Recent studies show that patients with Alzheimer's disease (AD) harbor specific methylation marks in the brain that, if accessible, could be used as epigenetic biomarkers. Liquid biopsy enables the study of circulating cell-free DNA (cfDNA) fragments originated from dead cells, including neurons affected by neurodegenerative processes. Here, we isolated and epigenetically characterized plasma cfDNA from 35 patients with AD and 35 cognitively healthy controls by using the Infinium MethylationEPIC BeadChip array. Bioinformatics analysis was performed to identify differential methylation positions (DMPs) and regions (DMRs), including ε4 genotype stratified analysis. Plasma pTau181 (Simoa) and cerebrospinal fluid (CSF) core biomarkers (Fujirebio) were also measured and correlated with differential methylation marks. Validation was performed with bisulfite pyrosequencing and bisulfite cloning sequencing. Epigenome-wide cfDNA analysis identified 102 DMPs associated with AD status. Most DMPs correlated with clinical cognitive and functional tests including 60% for Mini-Mental State Examination (MMSE) and 80% for Global Deterioration Scale (GDS), and with AD blood and CSF biomarkers. In silico functional analysis connected 30 DMPs to neurological processes, identifying key regulators such as and genes. Several DMRs were annotated to genes previously reported to harbor epigenetic brain changes in AD (, , , , , ) and were linked to ε4 genotypes. Notably, a DMR in the gene, previously shown to be hypermethylated in the AD hippocampus, was validated in cfDNA from an orthogonal perspective. These results support the feasibility of studying cfDNA to identify potential epigenetic biomarkers in AD. Thus, liquid biopsy could improve non-invasive AD diagnosis and aid personalized medicine by detecting epigenetic brain markers in blood. - Source: PubMed
Publication date: 2025/04/05
Macías MónicaAlba-Linares Juan JoséAcha BlancaBlanco-Luquin IdoiaFernández Agustín FÁlvarez-Jiménez JohanaUrdánoz-Casado AmayaRoldan MirenRobles MaitaneCabezon-Arteta EnekoAlcolea DanielGordoa Javier Sánchez Ruiz deCorroza JonCabello CarolinaErro María ElenaJericó IvonneFraga Mario FMendioroz Maite