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
- Cyclin-dependent kinases (CDKs) play a crucial role in cell cycle (such as CDK1 and CDK4/6) and transcription (such as CDK7, CDK9, and CDK12/13). While CDK inhibitors are clinically effective in cancer therapy, their mechanisms of apoptosis induction remain incompletely understood. Here, we demonstrate that inhibition of CDKs involved in cell cycle control (such as CDK1 or CDK4/6) displays no cytotoxic potential. Surprisingly, inhibition of CDK7, which is involved in the control of cell cycle and transcriptional initiation, also showed no cytotoxicity. Only inhibition of CDK9 (by AZD4573 and atuveciclib) or of CDK12/13 (by SR4835 and THZ531)-which target the transcriptional elongation of RNA polymerase II (RNAPII)-exerted a strong apoptotic potential. Since CDK9 and CDK12/13 target different elongation factors associated with RNAPII (such as SPT6 and NELF for CDK9; CDC73, and LEO1 for CDK12/13), they cannot substitute for each other. Consequently, the combination of AZD4573 with SR4835 resulted in significant, synergistic cytotoxicity. Inhibiting CDK9 or CDK12/13 induced the rapid downregulation of the short-lived, anti-apoptotic Bcl-2 proteins Mcl1 and A1/Bfl1 in Jurkat leukemia cells and SUDHL1 lymphoma cells, whereas the expression of Bcl-2 and Bcl-xL remained unaffected. Since Mcl1 and A1 antagonize the pro-apoptotic Bcl-2 proteins Bak and Bax, apoptosis induction by AZD4573 or SR4835 was blocked in Bak- and Bax/Bak-deficient Jurkat cells and strongly reduced in Bax-deficient cells. Because Bcl-2 only inhibits Bax, but not Bak, AZD4573 and SR4835 were able to induce apoptosis in Jurkat cells overexpressing Bcl-2. As tumor cells frequently upregulate Bcl-2, inhibitors of CDK9 and CDK12/13 represent promising anticancer drugs. - Source: PubMed
Publication date: 2026/05/27
Krings Karina SHatzfeld JudithWeller SandraBorkowski NadineLlewellyn Tanya RSchmitt LauraScherer BoItkonen Harri MPeter ChristophStork BjörnGeyh StefanieEickhoff JanKlebl BertQin NanEssmann FrankWesselborg Sebastian - : Excessive dietary inorganic phosphate (Pi) as a food additive poses potential health risks. : This study investigated the impact of excessive dietary inorganic phosphate on intestinal and immune homeostasis in mice using gradient Pi exposure combined with an inflammatory model. : Pi overload induced atrophy in the thymus, spleen, and kidney; damaged the intestinal barrier; reduced the villus height-to-crypt-depth ratio; and decreased goblet cell numbers. Altered levels of serum sIgA and IgE, as well as intestinal IgA, IgG, IgE, and IgM, together with decreased IFN-α, indicated altered levels of immunoglobulins and cytokines under Pi treatment. Proteomic analysis revealed differential expression of key proteins, including CNTFR and Bcl2l1 in the JAK/STAT pathway and metabolic regulators CPT1α and IDH1, when comparing Pi-treated mice with the control group. : These preliminary findings suggest that Pi may affect intestinal mucosal barrier function and systemic immune response through immune regulation and mitochondrial metabolic pathways, providing preliminary insight into the potential health implications of Pi overconsumption in humans. - Source: PubMed
Publication date: 2026/05/16
Sun ZongchaoHuang ShiyaZhao YuxinLuan YunhanWang YinuoWang RunzheWu WeiweiHuang DanliLiu JiankangZhang Yinghui - The HBx protein from Hepatitis B virus (HBV) is essential for replication and promotes pathogenicity during chronic infection. HBx hijacks host proteins, reprogramming them to evade antiviral defence. However, the structural basis of recruitment remains largely unknown. The HBx isoform derives from integration of viral DNA into the host genome and is linked to hepatocellular carcinoma. We present an NMR-based setup to characterize HBx-host protein interactions at residue-level resolution. HBx is disordered in isolation but undergoes local folding upon binding apoptosis regulator Bcl-xL and epigenetic reader Spindlin1. The HBx-Spindlin1 complex is bivalent: a hydrophobic interaction combines with a sticky patch realized via a rare inter-molecular zinc finger. HBx thus conceals the region responsible for recruiting Spindlin1 to histone tails, promoting transcription of extrachromosomal viral DNA. This mechanism exemplifies the capacity of HBx to engage diverse host factors into dynamic complexes. - Source: PubMed
Publication date: 2026/05/25
Clavier AlexisShida ToshinobuDroemer Maxim AGómez-Evain Santiagovon Hammerstein FranziskaHolzinger JulianLeuthold Mila MDouat CélineSchütz Anne K - B cell antigen receptor (BCR) signaling plays a critical role in regulating B cell fate, including activation, tolerance, and apoptosis. In immature B cells, strong BCR engagement induces apoptosis, which contributes to the elimination of autoreactive clones during negative selection. However, the molecular mechanisms linking BCR signaling to apoptotic pathways remain incompletely understood. In this study, we investigated the role of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in BCR-induced apoptosis using the immature B cell line WEHI-231. Stimulation of the BCR with anti-IgM antibody induced a rapid increase in intracellular Ca2+ levels and promoted apoptosis in WEHI-231 cells. BCR engagement also induced phosphorylation of CaMKII, indicating activation of this kinase downstream of Ca2+ signaling. Pharmacological inhibition of CaMKII with KN-93, a CaMKII inhibitor, attenuated BCR-induced apoptosis, whereas overexpression of CaMKII enhanced cell death. We further found that BCR stimulation resulted in downregulation of the anti-apoptotic protein Bcl-xL, and inhibition of CaMKII prevented this reduction. Conversely, CaMKII overexpression further enhanced Bcl-xL downregulation following BCR stimulation. Importantly, restoration of Bcl-xL expression significantly rescued CaMKII-mediated apoptosis. These findings identify a Ca2+-CaMKII-Bcl-xL signaling axis that promotes BCR-induced apoptosis in immature B cells. - Source: PubMed
Okubo RyosukeKajihara Ryutaro - Inflammation-induced pulmonary fibrosis is an irreversible and severe complication that leads to persistent decline in lung function and increased mortality; however, its early pathogenesis is still unclear. This study aimed to systematically elucidate the initiation mechanism of pulmonary fibrosis in the early stages of inflammation. By integrating multi-omics data and animal models, we found that lung exhibits stronger immune amplification and more severe mitochondrial dysfunction in comparison with other organs during inflammation, consequently fibrotic signaling is initiated in the acute phase. Mitochondria-related gene analysis identified six key genes (Bcl2l1, Gsr, Msrb3, AA467197, Stom, and Sod2) involved in the regulation of reactive oxygen species (ROS) metabolism, which were closely associated with clinical outcomes in sepsis. Temporal data and TNF-α/IL-1β intervention experiments revealed that these cytokines are persistently overexpressed in septic lungs, serving as critical drivers of ROS activation. In vitro assays further confirmed that ROS overload directly induces cellular damage and functional reprogramming of fibroblasts. Through bulk and single-cell transcriptomic analyses, we elucidated the alteration of intercellular communication between immune and parenchymal cells, and identified Col13a1 fibroblasts as a key subpopulation with the capability to drive fibrotic remodeling. In conclusion, sustained TNF-α/IL-1β signaling in septic lungs exacerbates ROS accumulation, thereby driving aberrant fibroblast repair and initiating pulmonary fibrosis, in which Col13a1 fibroblasts represent the major profibrotic subpopulation. Thus, the early inhibition of TNF-α/IL-1β expression, suppression of ROS accumulation, and regulation of Col13a1 fibroblast activation may provide an effective therapeutic strategy for sepsis. - Source: PubMed
Publication date: 2026/05/16
Zhong ZhaoqianWu KanWang JunhaoChen GuimingLuo HaihuaChen GuangqinSun ChangGuo DanyanLi LeyiLi LeiJiang Yong