ATG2B Antibody Autophagy Antibody
- Known as:
- ATG2B Antibody Autophagy Antibody
- Catalog number:
- AUT-7005
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ATG2B Antibody Autophagy
Related genes to: ATG2B Antibody Autophagy Antibody
- Gene:
- ATG2B NIH gene
- Name:
- autophagy related 2B
- Previous symbol:
- C14orf103
- Synonyms:
- FLJ10242
- Chromosome:
- 14q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-20
- Date modifiied:
- 2016-10-05
Related products to: ATG2B Antibody Autophagy Antibody
Related articles to: ATG2B Antibody Autophagy Antibody
- Langya chickens, a Chinese indigenous breed, exhibit rich genetic resources but relatively low egg production performance. To investigate the genetic basis of egg production traits, we performed low-depth genome resequencing of 1,183 Langya hens and evaluated six phenotypic traits, including age at first egg (AFE), egg number at different laying stages-EN1 (from first egg to 26 weeks), EN2 (27-36 weeks), EN3 (37-43 weeks), total egg number at 43 weeks (E43), and maximal clutch length (MCL). Genetic parameter analysis revealed that MCL exhibited high heritability (0.42) and strong genetic correlations with both egg production and AFE, suggesting its potential as a more effective selection indicator for egg production traits. Genome-wide association studies identified a total of 245 SNPs associated with these traits. Notably, a 6.58 Mb region on chromosome 5 (GGA5, 40.03-46.61 Mb) was enriched for multiple traits and in strong linkage disequilibrium. Candidate genes in this core region, including TSHR, GTF2A1, DIO2, STON2, NRXN3, KCNK10, EML5, and FOXN3, were implicated in transcriptional regulation, thyroid hormone signaling, neuroendocrine modulation, and ovarian function. Additional trait-specific candidate genes, such as ATG2B for EN2, FMNL1 for EN1/EN2, TDP1 for E43, and TPMT for MCL, were also identified. Functional enrichment analyses highlighted pathways related to cellular processes, lipid metabolism, and signal transduction. These findings provide genomic insights into the molecular mechanisms underlying egg production traits and offer valuable candidate genes for marker-assisted breeding in Langya chickens. - Source: PubMed
Publication date: 2026/01/04
Zhang HongruiFu YuanjieWang YanlinYin SijingJiang YunliangSun YiKang Li - Terminal erythroid differentiation (TED) is the maturation process of proerythroblasts into enucleated erythrocytes. Animal models are essential for studying red blood cell disorders. - Source: PubMed
Publication date: 2025/12/02
Tang Xiao-YueChen Jia-HuanYang RanFan HongYang KeDing TaoWang Qiao-ChuYang Ye-HongWu YueZhang Zhi-YiShi Chun-MeiLiu Xue-HuiLiu Jiang-FengLv XiangYang Jun-Tao - This study aimed to identify germline pathogenic variants in the and genes among patients with acute myeloid leukemia. The study included 92 patients with AML. A novel, likely pathogenic germline variant was identified in the gene in one patient. Additionally, germline variants of uncertain significance were detected in four patients: one in , two in , and one in . The median age at AML diagnosis was six years younger in patients carrying germline variants compared to those without. The identification of AML susceptibility genes enhances our understanding of the disease pathogenesis, aids help with recognizing in recognizing individuals at elevated risk, forms the basis for genetic counseling and patient management, assists in selecting suitable donors for allogeneic hematopoietic stem cell transplantation, and supports the development of targeted therapeutic strategies. - Source: PubMed
Publication date: 2025/10/27
Bąk AnetaPasińska MagdalenaJaśkowiec AnnaPotoczek StanisławCzyżewska MariaHaus Olga - Colorectal cancer (CRC), which has high mortality and increasing morbidity is a major concern worldwide. The autophagy pathway plays a crucial role in carcinogenesis and drug resistance in this disease. Epigenetic modification is one of the main regulatory mechanisms for this pathway. This study aimed to investigate the impact of promoter methylation as one of the epigenetic modifications on the expression of autophagy-associated genes (ATGs) ( and ) in 21 CRC patients from southern Iran. The tissue DNA and RNA were extracted by standard phenol-chloroform extraction method and A BIOZOL RNA isolation kit, respectively. The methylation status and transcript levels of desired genes were ascertained using the methylation-specific PCR and quantitative real-time PCR methods, respectively. In the majority of studied patients, the relative mRNA expressions of were significantly higher in CRC tissues compared to normal ones. There was no significant relationship between the methylation of the genes and clinicopathological features of CRC patients. Interestingly, in most of the patients, the promoter hypermethylation of the , , and genes led to their high mRNA expression. Although promoter hypermethylation usually suppresses gene expression, the cancer type, stage, and compensatory mechanisms may reverse this association. This highlights the complexity of the epigenetic regulation of , , and genes in CRC. Further large-scale studies will contribute to discovering the exact influences of methylation in CRC carcinogenesis and thereby may thereby provide novel targets and biomarkers for this lethal illness. - Source: PubMed
Niknam MaryamNaghibalhossaini FakhraddinHosseini Seyed VahidZamani MozhdehMokarram Pooneh - Intestinal barrier damage is crucial for the development of sepsis. Ghrelin (GHS) can restore intestinal barrier function. However, the mechanisms of GHS on intestinal barrier damage in sepsis remain unclear. We aimed to explore the mechanisms of GHS against intestinal barrier damage in sepsis. Septic models were established by cecal ligation and puncture surgery for rats and lipopolysaccharides exposure for IEC-6 cells. Furthermore, these septic models were overexpressed miR-143 and treated with GHS. In vivo, small intestinal pathological injury and D-lactic acid level were detected. Tight junction protein (Claudin-1, Occludin and ZO-1) expressions and autophagosome number were evaluated. In vitro, cell viability, autolysosome number, and relationship between miR-143 and ATG2B were determined. miR-143, ATG2B and autophagy-related protein (Beclin-1, p62 and LC3I/LC3II) levels were evaluated in rats and cells. GHS mitigated small intestinal pathological injury and decreased D-lactic acid level for septic rats. Additionally, GHS elevated tight junction protein expressions, ATG2B, Beclin-1 and LC3I/LC3II levels, and autophagosome number, but reduced miR-143 and p62 levels for septic rats. However, miR-143 overexpression presented the opposite results. Consistently, cellular experiments found that GHS increased cell viability, autolysosome number, and presented similar results for miR-143, ATG2B and autophagy-related protein levels for lipopolysaccharides-exposed cells. Additionally, ATG2B directly targeted miR-143 in IEC-6 cells. Both animal and cellular experiments found the effects of GHS on sepsis-induced small intestinal barrier damage were reversed by miR-143 overexpression. GHS may improve small intestinal barrier damage in sepsis through miR-143/ATG2B-mediated autophagy, indicating miR-143/ATG2B was an underlying therapeutic target for sepsis. - Source: PubMed
Publication date: 2025/08/07
Liu JingquanShi KaiCai HanhuiZheng ZihaoFan BinYang XianghongShao Ziqiang