BCL2L1 antibody - N-terminal region (ARP30475_T100)
- Known as:
- BCL2L1 (anti-) - N-terminal region (ARP30475_T100)
- Catalog number:
- arp30475_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- BCL2L1 antibody - N-terminal region (ARP30475_T100)
Related genes to: BCL2L1 antibody - N-terminal region (ARP30475_T100)
- 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 antibody - N-terminal region (ARP30475_T100)
Related articles to: BCL2L1 antibody - N-terminal region (ARP30475_T100)
- Breast cancer is a profound cause of mortality among women globally. Similar to BH3 mimetics, targeting the antiapoptotic Bcl-xL:Beclin1 protein complex is crucial to inducing apoptosis and autophagy, thereby suppressing tumor progression in breast cancer cells. This study aims to synthesize and evaluate a series of imidazopyridine-tethered pyrazoline drug prejudice-scaffold derivatives (5a-5l) as Beclin-1 mimetics that induce apoptosis and autophagy and mainly for their potential anticancer activity, focusing on the most potent compound 5c. The primary goal is to assess its ability of compound 5c to inhibit Bcl-xL:Beclin-1 interaction, thereby inducing a protective autophagic response subsequently to assess apoptosis to suppress breast cancer cell proliferation. Molecular docking studies were conducted to evaluate the binding affinity of compound 5c with Bcl-xL, and the interactions were visualized through a three-dimensional interaction map, highlighting key stabilizing interactions. Cytotoxic effects of compound 5c on MCF-7 breast cancer cells were assessed using alamarblue assay. To investigate the antiproliferative potential, colony formation, and wound healing assays were performed at varying concentrations. Apoptotic induction was analyzed through Western blotting for key proteins (BAX, Bcl-xL, Bcl-2), caspase-3/7 activation, and AnnexinV/PI assay using flow cytometry. Additionally, autophagy was examined by monitoring LC3B-I to LC3B-II conversion, Beclin-1 upregulation, and lysosomal activity using LysoTrackerRed staining. The involvement of compound 5c in autophagic flux was further confirmed by quantifying LC3-II accumulation in the presence of an autophagy inhibitor chloroquine (CQ), and then the effect of 5c-induced cell viability and apoptosis were evaluated and caspase-3/7 activity, respectively, during autophagy inhibition condition in MCF-7 cell line. A strong binding interaction of compound 5c with the hydrophobic groove of Bcl-xL demonstrated its potential as an effective Bcl-xL inhibitor. Compound 5c significantly reduced MCF-7 cell viability in a dose-dependent manner (IC50: 9.7 μM). The inhibitory effect of compound 5c on cancer cell proliferation and migration was observed. Treatment with compound 5c induced dose-dependent apoptosis in MCF-7 cells, as confirmed by Annexin V/PI using flow cytometric analysis after 72 h of exposure. A significant decrease in viable cells accompanied by an increase in apoptotic cell populations was observed with increasing concentrations of 5c. Upregulated BAX expression and downregulation in Bcl-xL and Bcl-2 expression levels indicated apoptosis induction. Caspase-3/7 activation further confirmed apoptotic cell death. Autophagy assessment revealed enhanced LC3B-II accumulation, Beclin-1 upregulation, and reduced p62 levels, suggesting modulation of autophagy. CQ treatment further increased LC3-II levels, indicating compound 5c-mediated autophagic flux induction and a significant reduction in cell viability and increased caspase 3/7 activity, confirming modultion of autophagy-dependent apoptosis by 5c. Similar to BH3 mimetic, compound 5c emerges as a promising small-molecule inhibitor targeting the Bcl-xL:Beclin-1 complex, which effectively induces apoptosis by modulating protective autophagy in breast cancer cells. Its dual mechanism of action highlights its potential as a novel therapeutic candidate for breast cancer treatment. - Source: PubMed
Shivakumar RashmiBeeraka Narasimha MOsmani Riyaz Ali MRavi Bhoomika BYadhav Monisha H SNagaraju DileepBhol Chandra SekharNagalakshmi AllakaAhn Kwang SeokNikolenko Vladimir NChinnathambi ArunachalamBender AndreasBasappa Basappa - Natural killer (NK) cells are promising candidates for cancer immunotherapy due to their safety and potent anti-tumor activity. However, their therapeutic efficacy is often limited by poor persistence and activity within the tumor microenvironment (TME) caused by a lack of essential cytokines. - Source: PubMed
Publication date: 2026/03/30
Wang ChunliKim SeokminKong Ling-ZuJang InhwanJo SeonaLee SunyoungLee Soo YunKim Kee KKim Tae-Don - Ageing and cellular senescence significantly contribute to the progression of age-related diseases, particularly chronic obstructive pulmonary disease (COPD). Cellular senescence refers to the cessation of cell division in response to stress and damage. While senescent cells remain metabolically active, they secrete pro-inflammatory factors that drive disease progression. Senolytic therapies aim to selectively target and eliminate these senescent cells by inducing their apoptosis. This study examines the senolytic potential of BCL-PROTAC, a novel proteolysis-targeting chimera designed to degrade BCL, in small airway epithelial cells and fibroblasts from patients with COPD. Treatment of COPD small airway epithelial cells and fibroblasts with BCL-PROTAC led to their apoptosis through the activation of caspase 3, along with a reduction in senescence markers such as p21, p16 and senescence-associated β-galactosidase. The effects of BCL-PROTAC were selective for senescent cells and did not affect non-COPD cells. The clearance of COPD small airway epithelial cells and fibroblasts by BCL-PROTAC was associated with an increase in the proliferation marker Ki67 and enhanced cell proliferation. Additionally, in precision-cut lung slices obtained from COPD patients, BCL-PROTAC significantly reduced p21 expression in the airway epithelium, validating its effectiveness in a more complex tissue environment. These findings demonstrate that BCL-PROTAC is a potent and selective senolytic agent that may promote lung cell rejuvenation, supporting its potential as a novel therapeutic strategy for age-related diseases, including COPD. - Source: PubMed
Devulder Justine VFenwick Peter SKolosionek EwaAl-Sahaf MayViola PatriziaLemaire RaphaelRazdan NeetuKudo HiromiSinadinos AnthonyOdqvist LinaDonnelly Louise EBarnes Peter J - Biomarkers that predict disease progression and treatment-free remission (TFR) would be of significant clinical value in chronic myeloid leukaemia (CML). We have previously shown that CIP2A levels at diagnosis can identify patients at increased risk of progression. One mechanism by which CIP2A acts is through upregulation of the anti-apoptotic gene BCL-XL. In this study, we evaluated BCL-XL mRNA expression as a diagnostic biomarker using samples from the SPIRIT2 and DESTINY clinical trials. In SPIRIT2, which compared imatinib and dasatinib as first-line therapies, high BCL-XL expression was associated with treatment failure, poor early molecular response, and lower rates of MR2 and MR3 achievement in patients treated with imatinib. In the DESTINY trial, which assessed treatment de-escalation and discontinuation, BCL-XL expression was significantly higher in patients who experienced molecular relapse compared to those achieving sustained TFR. Notably, increases in BCL-XL were detectable 6 to 8 months prior to molecular relapse, suggesting it may serve as an early biomarker of unsuccessful TFR. We now propose a clinical diagnostic toolkit combining CIP2A and BCL-XL biomarkers to stratify CML patients by the risk of disease progression and likelihood of achieving successful TFR. - Source: PubMed
Publication date: 2026/03/25
Basabrain Ammar AAustin Gemma MHolcroft Alison KApperley Jane FClark Richard EVaradarajan ShankarLucas Claire M - Adenomyosis is a heterogeneous uterine disorder characterized by the presence of endometrial tissue within the myometrium. Autophagy, a key homeostatic process involved in tissue remodeling and stress adaptation, has been inconsistently described in adenomyosis. This study aimed to define the temporal and compartment-specific regulation of autophagy-associated markers during disease progression, using a tamoxifen-induced CD1 mouse model and human uterine samples. - Source: PubMed
Publication date: 2026/03/25
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