BCL2L1 (phospho-Ser62) Antibody
- Known as:
- BCL2L1 (phosphorilated-Ser62) Antibody
- Catalog number:
- abx000362
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- BCL2L1 (phospho-Ser62) Antibody
Related genes to: BCL2L1 (phospho-Ser62) Antibody
- Gene:
- BCL2L1 NIH gene
- Name:
- BCL2 like 1
- Previous symbol:
- -
- Synonyms:
- BCLX, BCL2L, Bcl-X, bcl-xL, bcl-xS, PPP1R52
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-30
- Date modifiied:
- 2016-01-13
Related products to: BCL2L1 (phospho-Ser62) Antibody
Related articles to: BCL2L1 (phospho-Ser62) Antibody
- Bisphenol A (BPA) is a potential risk factor for pancreatic ductal adenocarcinoma (PDAC). This study integrated network toxicology, molecular docking, molecular dynamics (MD) simulations, and TCGA clinical data analysis to explore the potential molecular mechanisms linking BPA exposure to PDAC risk. BPA-PDAC intersection targets were identified through multi-database screening, followed by protein-protein interaction (PPI) network construction to screen core hub genes. A total of 10 core hub genes were identified via PPI analysis combined with the Maximal Clique Centrality (MCC) algorithm. Molecular docking demonstrated that ESR1 exhibited one of the strongest binding affinities for BPA (-8.2 kcal/mol), and MD simulations confirmed favorable thermodynamic stability of the BPA-ESR1 complex. TCGA analysis revealed stage-dependent expression patterns: early stages showed downregulation of TP53 and BCL2, whereas advanced stages showed upregulation of BCL2L1, HSP90AA1, and HSP90AB1, while ESR1, HIF1A, and PARP1 remained consistently low. These findings suggest that BPA may promote PDAC progression by disrupting ERα-mediated endocrine signaling and impairing DNA repair through PARP1 interference, providing candidate molecular targets and a hypothesis-generating foundation for pancreatic cancer risk assessment, warranting further experimental validation. - Source: PubMed
Publication date: 2026/07/20
Li XueruWu FanZhang ZunhanAn JiayiZhou GuoqiangWang YangZhao DandanChen Xiaolu - Nitro-aromatic compounds (NACs) are pervasive environmental pollutants with recognized pulmonary toxicity, yet their mechanistic involvement in pulmonary fibrosis remains incompletely understood. - Source: PubMed
Publication date: 2026/07/27
Yu HanmingLi MiaoKang XinDai YiLi FeiZhang YuanLi Qiuhong - Caspases are cysteine proteases that cleave specific proteins to control a range of cellular processes including cell death, inflammation, and differentiation. Proteomic approaches, like N-terminomics, have been central to identifying both cleaved proteins and where they are cleaved. We recently reported N-terminomics on differentiating and dying C2C12 myoblasts, identifying many new caspase substrates and cleavage sites. Here, we present a further analysis of this dataset demonstrating that there are caspase substrates "hidden" in our and in other N-terminomics datasets. We propose that for a subset of proteins, caspase cleavage is followed by removal of two amino acids from the neo-N-terminus by a dipeptidyl peptidase (DPP). As the peptide sequence of the neo-N-terminus is used to identify the cleavage site, this hides the caspase-mediated cleavage event. The implications of this are that N-terminomics datasets can be used to reveal hitherto unidentified caspase substrates and provide more information on cell-fate decisions. In C2C12 myoblasts, we have shown that cleavage of "hidden" substrates in apoptotic myoblasts that is absent from differentiating myoblasts (which also contain active caspase-3), suggesting that cleavage may identify apoptotic cells. A better understanding of the interplay between caspases and other proteases and their sequential action on caspase substrates may allow further elucidation of cell fate decisions. - Source: PubMed
Fotouhi FatemehGomez-Cardona ErikPatel JainilkumarJulien OlivierFearnhead Howard - Carbon nanotubes (CNTs) are carbon-based nanomaterials. They have been widely used in environmental technologies and in biomedical fields. - Source: PubMed
Publication date: 2026/07/01
Lotfipanah ShirinSaremi LeilaRafieitabatabaei YasaminsadatAsgari MasoudHajebrahimi Zahra - Starvation is a common stressor in aquaculture that can markedly affect intestinal health and function in fish. This study focused on yellow cheek carp (Elopichthys bambusa, initial body weight: 221.36 ± 6.75 g; initial body length: 28.47 ± 0.56 cm) to explore how short-term (8 days) and long-term (28 days) starvation influence intestinal morphology, expression of key functional genes, and gut microbiota composition. Additionally, Spearman's rank correlation analyses were conducted to explore potential host-microbe interactions. The results showed that short-term starvation did not significantly affect intestinal muscle layer thickness or villus height, but markedly upregulated genes associated with autophagy and apoptosis such as bcl-2-associated X protein 2 (bax2), bcl-2-like protein 1 (bcl2l1), and cysteine-aspartic acid protease 8(casp8). It also increased microbial diversity and altered the composition of dominant gut microbiota. In contrast, long-term starvation significantly suppressed the expression of copper/zinc superoxide dismutase (Cu-Zn sod), casp3a, and casp9, increased the number of goblet cells, inhibited muscle layer development, and weakened the correlation between gut microbes and host gene expression. In summary, short-term starvation appears to maintain intestinal homeostasis through activation of autophagy- and apoptosis-related pathways in conjunction with microbial restructuring. However, prolonged starvation inhibited muscularis development, increased goblet cell density, downregulated antioxidant and immune-related gene expression, and weakened the associations between the host and its microbiota. These findings provide new insights into starvation-induced physiological responses and contribute to gut health management strategies in aquaculture. - Source: PubMed
Publication date: 2026/07/18
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