Bcl-2 IHC Antibody
- Known as:
- Bcl-2 Immunohistochemistry Antibody
- Catalog number:
- IW-MA1004
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- IHC
- Gene target:
- Bcl-2 IHC Antibody
Related genes to: Bcl-2 IHC Antibody
- Gene:
- BCL2 NIH gene
- Name:
- BCL2 apoptosis regulator
- Previous symbol:
- -
- Synonyms:
- Bcl-2, PPP1R50
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: Bcl-2 IHC Antibody
Related articles to: Bcl-2 IHC Antibody
- Schistosomiasis remains an important zoonotic parasitic disease, and hepatic fibrosis is a major cause of chronic pathology following Schistosoma japonicum infection. In schistosomiasis, hepatic fibrosis is the major cause of severe pathological damage. However, during the long-term co-evolution and coexistence between Schistosoma parasites and their hosts, the parasite can modulate the host hepatic fibrotic process through extracellular vesicle (EV)-mediated cross-species communication. In this study, we identified an EV-derived microRNA from Schistosoma japonicum, sja-miR-2a-3p, that suppresses hepatic pathology in the host. Using transwell co-culture and EV-isolation experiments, we confirmed that the helminth-specific sja-miR-2a-3p could be transferred to hepatic stellate cells (HSCs) via EVs. Bioinformatic and dual-luciferase assays revealed that host BCL2, a major anti-apoptotic gene, is a direct target of sja-miR-2a-3p. In vitro, sja-miR-2a-3p overexpression suppressed HSC proliferation and migration and induced mitochondrial dysfunction, caspase-3/-7/-9 activation, and apoptosis. In vivo, administration of sja-miR-2a-3p agomir to S. japonicum-infected mice significantly downregulated hepatic BCL2 expression, enhanced HSC apoptosis, alleviated granuloma formation, collagen deposition, and inflammation. Collectively, our findings reveal that schistosome EV-delivered sja-miR-2a-3p attenuates liver fibrosis by promoting mitochondrial apoptosis and functionally suppressing HSC activation. This study supports sja-miR-2a-3p as a candidate antifibrotic molecule. - Source: PubMed
Publication date: 2026/08/14
Dong BowenZhu DanlinXiong JunhanSun YuanzhaoZhang RuitingFu ZhiqiangLiu JinmingZhong HaoranJin Yamei - Lactic acid bacteria and their metabolites have shown promising biological activities against different types of cancer, esspecially, colon cancer. In our previouse study, we extracted and optimized the production of a mixture of three oligosaccharides from Lactobacillus acidophilus DSMZ 20079 at the laboratory scale using statistical experimental designs and the active oligosaccharide HPLC fraction was identified as LA-EPS-20079. Also, the anticancer activity of the extracted LA-EPS-20079 against colon cancer CaCo-2 cell line was confirmed via the downregulation of the gene expression of Bcl2 and Survivin genes (6). In the present study, we produced a mixture of bioactive oligosaccharides from L. acidophilus DSMZ 20079 in 10 L bioreactor that maintained the anti-colon cancer against CaCo-2 cell line effects, which is a major transition towards the semi industrial level. To that end, a batch fermentation was carried out in a 10 L bioreactor under uncontrolled pH condition, starting at pH 6.0. During the fermentation process, the bacterial cell mass was increased exponentially with a constant specific growth rate (µ) of 0.07 h, reaching a maximum biomass of 6.93 g L at 44 h. Also, the concentration of the produced total exooligosaccharides gradually increased and reached a maximum concentration of 1461.43 µg mL at 40 h post-incubation. Furthermore, the glucose consumption rate was 1.21 g L h, while the LAB-oligosaccharide production rate reached 96.22 µg mL h. Moreover, oligosaccharides chemical composition was studied after scaling up the production process using 1D and 2D proton and carbon NMR, along with monomeric composition analysis. The results indicated that LAB-oligosaccharide is a mixture of oligosaccharides, not a single structure, and the mixture consists of three monomeric sugars; herein, we referred to the oligosaccharide mixture as LAB-oligosaccharide. Additionally, the anticancer activity of LAB- oligosaccharide was tested in samples collected from the bioreactor at 0, 12, 14, 16, 18, 20, 22, 24, 36, 40 and 44 h time points against the CaCo-2 cancer cell line. The results confirmed the in-vitro anticancer activity with maximum inhibition percentages of 72.01% and 81.7% after 22 and 24 h, respectively. On the other hand, to establish an environmentally friendly production process, we evaluated the efficacy of using the bacterial biomass residue after LAB- oligosaccharide extraction as a substrate for bacterial isolates growth to produce industrially important enzymes (Lipases and proteases). In this context, 5 bacterial isolates were found to produce both enzymes. These bacterial isolates were characterized using 16S-rRNA gene sequencing and the relatedness between the isolates was studied using phylogenetic analysis. The results demonstrated that the residual biomass supported the growth of B. subtillis PX205316 (2F) for the production of commercially valuable lipase and protease enzymes, hence, the recommended bioprocess was efficient in producing substrate with potential anticancer properties in a process that is environmentally friendly that promotes environmental sustainability. - Source: PubMed
Publication date: 2026/08/12
Kenawy Ahmed MAbo-Zaid Gaber ATaha Tarek HRagab Amany EAl-Madboly Lamiaa AEl-Deeb Nehal M - Polymyxins remain indispensable last-line antibiotics for multidrug-resistant Gram-negative infections, yet their clinical use in central nervous system (CNS) infections is constrained by poorly understood neurotoxicity. Here, we define the early molecular signalling events underlying polymyxin B-induced CNS toxicity using an integrated phosphoproteomic and Reverse Phase Protein Array (RPPA) approach in rat brain following intracerebroventricular administration. Global phosphoproteomics revealed extensive phosphosite coverage but identified a highly selective set of significantly regulated phosphosites, implicating calcium-dependent signalling, transcriptional stress regulation, synaptic signalling, and cytoskeletal control, while parallel total proteomics showed minimal changes in protein abundance. RPPA profiling independently confirmed coordinated modulation of stress, apoptotic and survival-associated signalling pathways, including p53, CREB, SQSTM1, Bcl-2, and NFκB related nodes. Network and functional enrichment analyses converged on DNA damage signalling, apoptotic regulation and growth factor-mediated pathways as central features of the polymyxin B early neurotoxicity response, while phosphor to total protein analyses demonstrated suppression of proliferative and pro-survival signalling. Together, these data establish phosphorylation-driven signalling reprogramming as a primary early mechanism of polymyxin B-induced neurotoxicity, providing a mechanistic framework that links membrane-active antibiotic exposure to neuronal stress signalling and identifies candidate pathways for toxicity biomarkers and neuroprotective strategies. - Source: PubMed
Publication date: 2026/08/14
Hussein MaythamAnsaf Thuraya SafaaSian Terry C C Lim KamBaker MarkFaridi PouyaKho Zhi YingSelvakumar NivedhithaKaye Keith SRao Gauri GLi JianVelkov Tony - Osteoporosis is a chronic disease driven by an imbalance between bone-building osteoblasts and bone-resorbing osteoclasts, whose hyperactivation can promote this condition. Osteoclasts are multinucleated cells, and their activity directly correlates with their ploidy level. Multinucleation associates with the accumulation of extra centrosomes that can activate the PIDDosome pathway. Depending on cell type, this can lead to a p53/p21-mediated cell cycle arrest, or BCL2-regulated apoptosis. Here, we report that the PIDDosome controls polyploidization in osteoclasts and its absence triggers bone erosion in mice. PIDDosome activation in osteoclasts depends on the presence of extra centrosomes bearing the distal appendage protein ANKRD26. Consistently, loss of Ankrd26 phenocopies PIDDosome-deficiency in osteoclasts. Surprisingly, p53 and p21, which restrict cell cycle progression in the presence of extra centrosomes, are not involved in limiting osteoclast polyploidization and function. In support of this notion, bones from p53 mice display a higher trabecular bone mass phenotype, and osteoclasts generated from p21 mice show normal OC ploidy and function. Altogether, we document that the PIDDosome regulates bone homeostasis by regulating osteoclast polyploidization and their bone-resorbing function independently of the canonical p53/p21 axis, hinting towards unknown downstream effectors. We propose that modulation of PIDDosome activation might be therapeutically exploited for osteoporosis treatment, while its inhibition may ameliorate osteopetrosis symptoms. - Source: PubMed
Publication date: 2026/08/14
Leone MObwegs DKinz NMaccataio ADegenhart GLiguori RPetermann P YSladky V CEichin FRiley J SDorigatti IWatschinger KRizzotto DFerrazzi FSteffen UVillunger A - Chlorpyrifos (CPF), a widely used organophosphate insecticide, can cause intestinal toxicity under chronic exposure conditions, but the upstream mechanisms underlying intestinal epithelial barrier-associated injury remain unclear. This study investigated whether endoplasmic reticulum stress (ERS) contributes to CPF-induced tight junction (TJ) alterations and intestinal epithelial injury. We used an 8-week drinking-water exposure model in weaned ICR mice with 30, 60, and 120 mg/L CPF and a MODE-K cell model, combined with pharmacological ERS modulation using 4-phenylbutyric acid (4-PBA) and tunicamycin (TM). Quantitative single-cell immunofluorescence was performed at 12, 24, and 48 h to assess temporal changes in TJ proteins and apoptosis-related markers. CPF induced jejunal villus atrophy, reduced the villus-to-crypt ratio, downregulated ZO-1, Occludin, and Claudin-1, impaired TJ structural integrity, increased the total protein levels of PERK, IRE1, and ATF6, and enhanced apoptosis-related alterations, including increased Bax and total Caspase-3 levels and decreased Bcl-2 levels. 4-PBA partially restored TJ protein expression and attenuated apoptosis-related alterations, whereas TM further aggravated TJ protein loss and apoptosis-related changes. Time-course analysis showed that TJ protein reductions were detectable before marked apoptosis-related changes and persisted at later time points. Collectively, chronic CPF exposure induced jejunal epithelial barrier-associated injury in weaned mice, accompanied by coordinated increases in the total protein levels of UPR sensors, TJ protein reductions, and enhanced apoptosis-related alterations. The opposing effects of 4-PBA and TM support the involvement of ERS in CPF-associated epithelial injury. These findings suggest that ERS contributes to progressive intestinal epithelial injury induced by CPF. - Source: PubMed
Publication date: 2026/08/14
Zhao JunkangZhang YueLi JinyuZhu YuliSong XunuoMeng YaoZhang YumingDeng QinghuaDu Liyin