ELISA Human , Bcl-2
- Known as:
- Enzyme-linked immunosorbent assay test Human , Bcl-2
- Catalog number:
- RBMS244/3R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Human Bcl-2
Related genes to: ELISA Human , Bcl-2
- 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: ELISA Human , Bcl-2
Related articles to: ELISA Human , Bcl-2
- Whether PM2.5-induced spermatocyte injury engages the cGAS-STING innate immune pathway remains unknown. This study integrated network pharmacology, GEO transcriptomic profiling (GSE189187), gene set enrichment analysis, molecular docking with positive-control benchmarking, single-cell RNA sequencing, and in vitro validation in GC-2 spermatocyte cells to address this question. Among 35 overlapping candidates between 447 AS-IV putative targets and 102 cGAS-STING/inflammation genes, Hmox1 was the sole gene significantly upregulated by PM2.5 (log₂FC = 2.15, AUC = 1.000). KEGG analysis identified six enriched innate immunity pathways, with the Cytosolic DNA-sensing pathway at adjusted P = 8.1 × 10⁻⁶. Molecular docking demonstrated that AS-IV bound cGAS (-10.2kcal/mol) and STING (-11.3kcal/mol) with affinities exceeding known inhibitors G150 (-8.8) and H-151 (-8.6). In GC-2 cells, PM2.5 (200μg/mL) increased ROS 5.35-fold, elevated apoptosis to 42.83%, and activated cGAS-STING signaling. AS-IV co-treatment restored viability to 83.3%, enhanced proliferation to 37.96%, significantly suppressed cGAS/p-TBK1/p-IRF3, and activated Nrf2/HMOX1 (HMOX1 protein 1.99 ± 0.05-fold; mRNA 6.44-fold), reducing apoptosis to 18.27%, ROS, and LDH release, and normalizing the Bax/Bcl2 ratio from 5.0 to 2.1. These findings establish that AS-IV protects spermatocytes through coordinated cGAS-STING suppression and Nrf2-dependent HMOX1 activation. Causal necessity of cGAS-STING activation was confirmed by RU.521-mediated pathway blockade, and direct AS-IV binding to cGAS (KD = 0.619μM) and STING (KD = 0.097μM) was validated by surface plasmon resonance. - Source: PubMed
Publication date: 2026/08/18
Jin JinZhang Congxue - Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive hematologic malignancy with complex clinical manifestations, frequently involving multiple organs. Treatment of BPDCN has evolved over the years from conventional chemotherapy to novel targeted therapies including anti-CD123 antibody drug conjugates, namely tagraxofusp and pivekimab sunirine, and the BCL-2 inhibitor, namely venetoclax. However, because anticipated long term disease control is not generally possible, it is standard practice to offer allogeneic hematopoietic cell transplantation (HCT) as a consolidation strategy for eligible patients. No HCT societal guidelines exist to guide contemporary clinical practice of HCT in patients with BPDCN. A panel of 17 experts, including one representative of community practice, was convened to develop relevant guidelines and followed the Grading of Recommendations, Assessment, Development and Evaluation methodology. For BPDCN in first complete remission (CR1), the panelists recommended allogeneic HCT and suggested autologous HCT for patients who are unfit for allogeneic HCT but without BPDCN marrow involvement. Acknowledging that some patients might not have received either allogeneic or autologous HCT in CR1, panelists voted similarly for patients in second CR (CR2). Conversely, the panelists did not recommend allogeneic or autologous HCT in BPDCN after primary induction failure or with active relapsed-refractory disease. The panel recommended that conditioning intensity for younger fitter patients be myeloablative, preferentially containing total body irradiation, whereas reduced intensity conditioning was recommended for older and/or frail ones, in both CR1 or CR2. Post-HCT intrathecal chemotherapy was also recommended regardless of involvement of the central nervous system. Panelists recognized that other unique clinical scenarios not included in these recommendations might demand individualized treatment approaches. - Source: PubMed
Publication date: 2026/08/18
Kharfan-Dabaja Mohamed AKumar AmbujPemmaraju NaveenMurthy HemantMalki Monzr AlBashir QaiserBubis JeffreyLane Andrew ANishihori Taigade Lima MarcosGangat NaseemaJamy OmerKonopleva MarinaLuger SelinaSavani BipinSweet KendraWang EuniceCarpenter Paul AHamadani Mehdi - Cardiotoxicity remains a major limitation of current anticancer therapies, highlighting the need for agents that combine antitumor efficacy with intrinsic cardiac safety. Phenotypic screening of a pyrimidine-based compound library identified compound 9v as a potent anti-prostate cancer candidate with dual biological functions. Compound 9v inhibited PC-3 cell proliferation with an IC₅₀ of 3.96 ± 0.18 μM, outperforming 5-fluorouracil, and markedly suppressed colony formation and migration while inducing apoptosis. Mechanistic studies showed that 9v activated the mitochondrial apoptotic pathway by increasing Bax, cleaved caspase-9, and cleaved caspase-3 levels while reducing Bcl-2 expression. Remarkably, 9v exerted bidirectional regulation of ROS homeostasis, promoting ROS accumulation in PC-3 cells but suppressing oxidative stress in H9C2 cardiomyocytes under H₂O₂ challenge. In addition, 9v exhibited weak cytotoxicity toward normal prostate stromal cells, no obvious acute toxicity in mice, and no detectable cardiotoxicity in vitro. Moreover, it exhibited protective effects against oxidative injury in cardiomyocytes, as demonstrated by increased cell viability and decreased LDH and cTnT release. Taken together, these results identify 9v as a promising lead compound with both anti-prostate cancer activity and cardioprotective potential in an in vitro oxidative stress model, providing a basis for the development of multifunctional anticancer agents with improved cardiovascular safety. - Source: PubMed
Publication date: 2026/08/13
Cao YaquanWu YaxiLi YunfeiLi ShuyaYoussif Bahaa G MDu JingxiaMa Liying - Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage destruction and loss of chondrocyte homeostasis. Although dysregulated autophagy contributes to OA pathogenesis, the molecular mechanisms governing autophagy-associated responses in chondrocytes remain incompletely understood. This study investigated the role of the miR-590-5p/SPRY2 regulatory axis in an inflammatory OA microenvironment using IL-1β-induced C28/I2 human chondrocytes. An in vitro OA model was established by treating C28/I2 cells with IL-1β. The expression of miR-590-5p and SPRY2 was evaluated using quantitative PCR and Western blotting. Gain- and loss-of-function approaches were employed to assess the effects of SPRY2 and miR-590-5p on the autophagy-associated markers Beclin-1 and LC3-II, as well as the survival-related protein Bcl-2. Bioinformatic analysis and rescue experiments were used to investigate the regulatory relationship between miR-590-5p and SPRY2. IL-1β treatment significantly increased miR-590-5p expression while reducing SPRY2 mRNA and protein levels (P < 0.05). SPRY2 overexpression markedly decreased Beclin-1 and LC3-II expression, with reductions of approximately 65% and 77%, respectively (P < 0.05). In contrast, miR-590-5p overexpression increased Beclin-1, LC3-II, and Bcl-2 expression, whereas inhibition of miR-590-5p reversed these effects and restored SPRY2 expression. Functional analyses supported SPRY2 as a putative downstream regulatory target of miR-590-5p. These findings identify the miR-590-5p/SPRY2 axis as an important regulator of autophagy-associated marker expression and chondrocyte survival under inflammatory conditions and suggest its potential relevance as a therapeutic target in OA. - Source: PubMed
Publication date: 2026/07/31
Mei QijieXu WenfeiWang ShunGuo JinrongYuan ChangshenZeng ChaoZheng HaijunDuan Kan - Glutamate-induced excitotoxicity is one of the key pathological mechanisms in neurodegenerative disorders, contributing to memory impairment, oxidative stress, and progressive neuronal degeneration. Caffeine has demonstrated neuroprotective properties by reducing oxidative damage and modulating hippocampal neuronal apoptosis. Intranasal (IN) administration provides a non-invasive and efficient route for direct brain delivery, minimizing systemic exposure and side effects. This study investigated the neuroprotective effects of IN caffeine in a monosodium glutamate (MSG)-induced excitotoxicity model. - Source: PubMed
Publication date: 2026/08/18
Hamzeh OliaPourabdolhossein FereshtehFeizi FaridehEsmaeili ZohreShanehbandpour-Tabari FarzaneBaghershiroodi MahnazPourbagher RoghayehRostami-Mansoor SaharNajafzadehvarzi Hossein