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抗Human BCL2L1 抗体:
抗Mouse (Murine) BCL2L1 抗体:
抗Rat (Rattus) BCL2L1 抗体:
Human Polyclonal BCL2L1 Primary Antibody for IHC, WB - ABIN6711678
Lu, Tang, Guo, Ren, Zhao: Sorafenib induces growth inhibition and apoptosis of human chondrosarcoma cells by blocking the RAF/ERK/MEK pathway. in Journal of surgical oncology 2011
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Human Polyclonal BCL2L1 Primary Antibody for ELISA, IF (p) - ABIN675129
Wang, Ma, Su: NF-?B pathway contributes to cadmium-induced apoptosis of porcine granulosa cells. in Biological trace element research 2013
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Human Polyclonal BCL2L1 Primary Antibody for IHC (p), WB - ABIN5518741
Zhou, Zhang, Li, Hao, Liu, Wang: Azithromycin synergistically enhances anti-proliferative activity of vincristine in cervical and gastric cancer cells. in Cancers 2013
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Human Polyclonal BCL2L1 Primary Antibody for IP, WB - ABIN223050
Cordiali-Fei, Ardigo, Mastroianni, Giuliani, D Agosto, Bordignon, Trento, Vento, Berardesca: Serum cytokines and biohumoral immunological characterization of psoriatic patients in long term etanercept treatment. in International journal of immunopathology and pharmacology 2008
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Human Polyclonal BCL2L1 Primary Antibody for FACS - ABIN5693068
Cui, Li, Xu, Zhang, Sun, Chen: Emodin alleviates severe acute pancreatitis-associated acute lung injury by decreasing pre-B-cell colony-enhancing factor expression and promoting polymorphonuclear neutrophil apoptosis. in Molecular medicine reports 2018
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Human Polyclonal BCL2L1 Primary Antibody for WB - ABIN541232
González-García, Pérez-Ballestero, Ding, Duan, Boise, Thompson, Núñez: bcl-XL is the major bcl-x mRNA form expressed during murine development and its product localizes to mitochondria. in Development (Cambridge, England) 1995
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Human Polyclonal BCL2L1 Primary Antibody for IP, WB - ABIN549109
Giuliani, Mioni, Altavilla, Leone, Bazzani, Minutoli, Bitto, Cainazzo, Marini, Zaffe, Botticelli, Pizzala, Savio, Necchi, Schiöth, Bertolini, Squadrito, Guarini: Both early and delayed treatment with melanocortin 4 receptor-stimulating melanocortins produces neuroprotection in cerebral ischemia. in Endocrinology 2006
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Human Polyclonal BCL2L1 Primary Antibody for IHC - ABIN965653
Cheng, Levine, Boise, Thompson, Hardwick: Bax-independent inhibition of apoptosis by Bcl-XL. in Nature 1996
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Human Monoclonal BCL2L1 Primary Antibody for FACS - ABIN135024
Chittenden, Harrington, OConnor, Flemington, Lutz, Evan, Guild: Induction of apoptosis by the Bcl-2 homologue Bak. in Nature 1995
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cytoplasmic apoptotic function of p73 is mediated through a noncanonical mode of Bcl-XL recognition
HSPA6 is a cigarette smoke-induced ulcerative colitis (UC)-susceptibility gene. The HSPA6 risk locus is associated with decreased HSPA6 expression. HSPA6 provides epithelial protection by stabilizing anti-apoptotic Bcl-XL, thereby contributing to the beneficial effect of cigarette smoking in UC.
our findings identify let-7b as a key regulator in platelet apoptosis by demonstrating let-7b targeting of Bcl-xL. Increasing let-7b expression during storage downregulates expression of antiapoptotic Bcl-xL and ultimately frees Bak to induce platelet apoptosis.
The inhibition of MCL-1, BCL-XL, and FGFR1 to maximize therapeutic response in FGFR1-expressing lung SqCC.
Examined the roles of BCL2 proteins in the induction of apoptosis in cells upon infection with flaviviruses, such as Japanese encephalitis virus, Dengue virus and Zika virus. Showed that survival of the infected cells depends on BCLXL, a pro-survival BCL2 protein due to suppression of the expression of another pro-survival protein, MCL1.
Bcl-xL abrogates the cytotoxic effects of LRRK2 inhibition in a neuroblastoma cell line (SH-SY5Y/Bcl-xL) overexpressing Bcl-xL.
E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death.
Study shows that multiple ion transporters mediate the rise in pH that increases the rate of Bcl-xL deamidation in response to DNA damage in certain cells. Additionally, deamidation of Bcl-xL is intramolecularly catalyzed in a manner that is dependent upon two conserved histidines near each of the deamidation sites and that they may function together as a pH-sensitive switch.
hTERT contains a BH3-like motif, a short peptide sequence found in BCL-2 family proteins, and interacts with anti-apoptotic BCL-2 family proteins MCL-1 and BCL-xL
Study demonstrated that lncRNA-HEIH regulates miR-939 expression through transcriptional repression of Bcl-xL promoting colorectal tumorigenesis.
Results showed that the expressions of RIP2 and BclxL were positively correlated with the malignant grade of astrocytoma. RIP2 promoted human glioblastoma cell proliferation by inducing expression of BclxL.
BCL-XL has a role in modulating RAS signalling to favor breast cancer cell stemness
Bcl-xL degradation during endoplasmic reticulum stress-induced apoptosis is mediated by RNF183.RNF183 ubiquitinates Bcl-xL.
BCL-XL promotes stemness and contributes to the aggressiveness of both melanoma and glioblastoma.
inhibition of the BCL2 family member BCLxL resulted in nanomolar potency against human synovial sarcoma cell lines and 50% tumor reduction in a genetically engineered mouse model
In this study, we investigated whether APG-1252-12A inhibits the growth of five leukemia cell lines in a concentration- or time-dependent manner by MTS assay.APG-1252-12A is a Bcl-2 homology (BH)-3 mimetic that specifically binds to Bcl-2 and Bcl-xl, which has shown efficacy in some Bcl-2 dependent hematological cancers
inhibition of Bcl-xL induces significantly more apoptosis in IDH1-mutated cells than in wild-type IDH1 cells.
CCAT1 is upregulated in docetaxel-resistant lung adenocarcinoma cells; its oncogenic function depends on sponging of let-7c, which releases Bcl-xl, promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes
In the epithelial ovarian cancer stem cells, 40% knock-down of Bclxl expression was sufficient to induce the full activation of caspases. Bclxl expression levels in EOC cells is dynamic and can be regulated by microenvironments that are enriched with the pro-inflammatory cytokine IL-6 such as the cancer stem cell and adipocyte niches.
Study reports the interaction of BCL-XL with RASSF6. BCL-XL inhibits the interaction between RASSF6 and MDM2 and suppresses p53 expression. Consequently, BCL-XL antagonizes RASSF6-mediated apoptosis. Thus, the inhibition of RASSF6-mediated apoptosis also underlies the prosurvival role of BCL-XL.
Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy.
targeting BCLxL in human and mouse synovial sarcoma with the small molecule BH3 domain inhibitor, BXI-72, achieved significant cytoreduction and increased apoptotic signaling.
GATA-3 participates in the healing of bone fractures via regulating bcl-xL gene expression, owing to its association with Runx2.
this study demonstrates that necrosis of Mycobacterium tuberculosis-infected macrophages is dependent on the action of Bcl-xl
Mitochondrial Bcl-xL is involved in maintaining mitochondrial respiratory capacity. Its deficiency causes oxidative stress, which is associated with an increased glycolytic capacity and balanced by an increased activity of the pentose phosphate pathway.
Proapoptotic proteins BIM and PUMA are not critical for the reticulocyte apoptosis caused by loss of the pro-survival protein BCL-XL.
BMP4 promotes survival of neural stem/progenitor cells by enhancing the anti-apoptotic function of Bcl-xL via BMP4-Smad1/5/8-Id1 signaling in the presence of FGF-2.
We propose that the GC-induced mitochondrial accumulation of Bax and the interaction between the GR and Bim, Bcl-xL and Bak could play a role in the regulation of thymocyte apoptosis.
Bcl-xL is required for survival of post mitotic neurons throughout the developing spinal cord.
anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.
Atherosclerosis-associated endothelial cell apoptosis may partially result from downregulation of Bcl-Xl, through upregulation of miR-876 that binds and suppresses translation of Bcl-Xl mRNA.
Bcl-xL is a driver in colorectal tumorigenesis and cancer progression.
These data show that Mcl-1 is dispensable for the regulation of apoptosis during infection with different large DNA viruses.Bcl-XL, on the other hand, can be important to maintain survival of virus-infected cells
BCL-XL expression promotes survival of immature B cells, expression of BCL-2 is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 is important for survival throughout B-cell development.
Bcl-xL deficiency induced apoptosis in a select population of differentiated neurons and led to severe neurobehavioral abnormalities.
loss of PUMA had no impact on the loss of platelets caused by loss of BCL-XL. It therefore remains to be established whether other BH3-only proteins play a critical role in induction of apoptosis in platelets or whether their death is controlled solely by the interactions between BCL-XL with BAK and BAX.
MLF1 is negatively regulated by 14-3-3 via binding to, and blocking, MLF1's Bcl-2 homology domain 3 and thereby preventing Bcl-XL from associating with MLF1.
Genetic and pharmacological inhibition of BCL-W and BCL-XL causes directed elimination of senescent cells.
amplification and characterization of partial regions of exons 2 and 3 of the bovine BCL2L1 gene
chromosome mapping by in situ hybridization.
Data show that Bcl-x(L) expression is increased in the pulmonary artery undergoing chronic pulmonary vascular remodeling.
interleukin-6, endothelin ET-1, and apoptotic Bak and Bcl-XL genes have roles in small bowel transplantation, in a swine model of ischemia and reperfusion injury
Bcl-xL was significantly decreased in haploid parthenotes compared with the diploid parthenotes. These results suggest that the haploid state affects apoptosis-related gene expression which results in increased apoptosis
CONCLUSION(S): (1) Apoptosis is involved in follicular atresia; (2) Bcl-2 is induced by warm ischemia; and (3) cryopreservation insult does not alter the apoptotic signals with short tissue preparation time.
Data show that cysteine significantly reduced the expression of pro-inflammatory cytokines, including TNF-alpha, IL-6, IL-12p40, IL-1beta, and resulted in increased expression of the apoptosis initiator caspase-8 and bcl2L1.
This study leads to conclude that BCLXL peak expression at the zygotic genome activation phase may be a requirement for embryo development
In this study evidence is provided that exogenous PGF2alpha differentially modulates luteal expression of BCL2L1 transcripts and protein depending on luteal stage.
repression of radiation-induced apoptosis by overexpression of Bcl-xL during embryonic development depends upon the timing of its expression and post-translational events that enable the protein to become effective
The bcl2l gene operates in the inhibition of cell death under direct regulation of a thyroid specific set of transcription factors
Zebrafish anti-apoptotic gene Bcl-xL can prevent aquatic birnavirus-induced cell death in fish cells without affecting expression of viral proteins.
transgenic overexpression of zfBLP1 or myeloid cell leukemia sequence 1a in zebrafish larvae interrupts regulation of the homeostatic balance between cell proliferation and programmed cell death during hepatogenesis and leads to liver hyperplasia
Bcl-xL can block post-apoptotic necrosis processes thereby rescuing betanodavirus-infected cells
Delta113p53 functions to antagonize p53-induced apoptosis via activating bcl2L
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The proteins encoded by this gene are located at the outer mitochondrial membrane, and have been shown to regulate outer mitochondrial membrane channel (VDAC) opening. VDAC regulates mitochondrial membrane potential, and thus controls the production of reactive oxygen species and release of cytochrome C by mitochondria, both of which are the potent inducers of cell apoptosis. Two alternatively spliced transcript variants, which encode distinct isoforms, have been reported. The longer isoform acts as an apoptotic inhibitor and the shorter form acts as an apoptotic activator.
apoptosis regulator Bcl-X
, bcl-2-like protein 1
, protein phosphatase 1, regulatory subunit 52
, B-cell leukemia/lymphoma x
, anti-apoptosis regulatory protein
, B cell lymphoma 2 like
, B cell lymphoma like X
, BCL2-like protein 1
, anti-apoptotic Bcl-xL
, BCLX protein
, BCL2-like 1
, apoptosis regulator R11
, Bcl-xL-like protein 1