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
- Mammary myofibroblastoma (MFB) is a rare benign mesenchymal tumor of the breast with myofibroblastic differentiation. Its diverse morphological spectrum may pose diagnostic challenges, particularly in limited biopsy specimens. All MFB patients diagnosed at a tertiary care center between 2015 and 2024 were reviewed retrospectively. Eleven patients were identified, including 7 women and 4 men, with a mean age of 56.5 years (range: 31-75 years). All patients presented with a solitary, painless breast mass. Tumor size ranged from 2.3 to 14 cm. Histologically, 9 tumors showed spindle cell morphology, whereas 2 showed epithelioid features. The common findings included short intersecting fascicles of bland spindle cells, variable collagen deposition, ectatic blood vessels, and focal adipocytic components. Immunohistochemically, CD34 was positive in 9 tumors, desmin in 8, smooth muscle actin (ACTA2) in 5, BCL2 and CD99 in 7 each, and CD10 in 4 tumors. Keratin AE1/AE3, p63, S100, and STAT6 were negative in all tumors. Follow-up data was available in 9 patients and no recurrence was reported. Recognition of its characteristic morphological and immunohistochemical features is essential to avoid diagnostic pitfalls. Complete surgical excision is curative, with an excellent prognosis. - Source: PubMed
Publication date: 2026/09/24
Naveed HaniaIdrees RomanaSafdar FatimaDin Nasir UdKayani Naila - To clarify the pathway by which electroacupuncture (EA) at "Taichong" (LR3) and "Zusanli" (ST36) alleviates low-grade duodenal inflammation in functional dyspepsia (FD) rats via regulating the Hippo/Yes-associated protein (YAP) signaling pathway. - Source: PubMed
Liang TingtingZhao YuWang TianlangZhang JiahaoWang XihanWang XiningFeng YifanGuo YueLiu YunxiaoQu YiXue YananLiu Jidong - Ficus carica fruit extract (FCFE) was evaluated for its cytotoxic and apoptotic effects against C6 glial cells. FCFE has been traditionally used for the treatment of neurodegenerative diseases. - Source: PubMed
Publication date: 2026/09/23
Thangaiyan RadhigaDhanabalan KarthikVeeramani ChinnaduraiAlsaif Mohammed AAl-Numair Khalid S - Acute myeloid leukemia (AML) remains difficult to treat because profound molecular heterogeneity enables rapid adaptive resistance to targeted therapy. We developed an AI-driven pharmacogenomic pipeline that integrates genomic, transcriptomic, epigenetic, and clinical features to predict patient-specific response to venetoclax and translate resistance-associated signals into actionable therapeutic hypotheses. Across internal and external cohorts, the deep learning model showed strong discrimination and generalization (AUROC 0.84-0.90), produced calibrated probabilities, and stratified overall survival independent of standard prognostic factors. Explainable modeling (SHAP) identified mechanistically coherent drivers of sensitivity and resistance: high BCL2 and apoptotic priming favored response, whereas MCL1 upregulation, TP53 disruption, and RAS/MAPK activation were dominant resistance programs. Translating these findings into therapy design, network-based modeling and in silico perturbation prioritized rational combinations expected to block escape routes, including venetoclax plus MCL1 inhibition (e.g., AZD5991-class inhibitors), venetoclax plus FLT3 inhibition (e.g., gilteritinib-class agents) in signaling-driven disease, and venetoclax plus p53-axis modulation (e.g., MDM2 inhibition) in TP53-altered contexts. Structural candidate evaluation using ensemble docking provided supportive drug-target interaction evidence for prioritized dependencies. Together, these results establish a clinically interpretable, resistance-aware AI framework for precision optimization of venetoclax-based combination therapy in AML. - Source: PubMed
Publication date: 2026/09/10
Wang ChenYou ZhijieChen SiqiHe YihuiChen XinQu ShuangChen XinJiang Sicong - Influenza A virus (IAV) exploits host pathways to maximize progeny production. Sulfatide, a sulfated glycosphingolipid on the plasma membrane, has been implicated in enhanced influenza replication; however, the underlying host factors remain unclear. Using sulfatide-low COS7 cells, sulfatide-enriched SulCOS1 cells, and Madin-Darby canine kidney (MDCK) cells that endogenously express sulfatide, we observed higher infectious viral yields in MDCK and SulCOS1 cells than in COS7 cells, without a corresponding increase in the number of initially infected cells. IAV infection triggered time-dependent activation of mitogen-activated protein kinase (MAPK) signaling in sulfatide-enriched cells, with a prominent response in extracellular signal-regulated kinases 1 and 2 (ERK1/2). Treatment with U0126, a mitogen-activated protein kinase kinase (MEK)/ERK-pathway inhibitor, reduced viral output without a marked increase in lactate dehydrogenase (LDH) release, although ERK dependence remains unresolved. To assess mitochondrial apoptosis-related responses, we examined the pro-apoptotic BH3-only protein Bim. In sulfatide-enriched SulCOS1 cells, Bim abundance decreased during the late phase of infection, whereas Bim remained relatively stable in COS7 cells. In MDCK cells, U0126 tended to preserve Bim abundance after infection. Although caspase-3 was activated after infection, pan-caspase inhibition did not detectably reduce hemagglutination (HA) titers under the tested conditions. In addition, changes in Bcl-2 family protein abundance were observed in MDCK and SulCOS1 cells, and Bax-targeting peptides increased influenza A and B virus production in MDCK cells. Together, these data support a model in which sulfatide-associated MEK/ERK signaling, Bim-related mitochondrial checkpoint changes, and other downstream processes may collectively contribute to efficient influenza virus production. - Source: PubMed
Publication date: 2026/09/23
Onishi ShintaroKurebayashi YukiTakahashi TadanobuHaraguchi NaotoSaito YuNishiie AnjuTsukamoto YoheiTakeuchi HideyukiMori TakuyaSuzuki Takashi