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Validated All-in-One™ qPCR Primer for BCL2L11(NM_138621.4) Search again
Product ID:
HQP000029
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BAM, BIM, BOD
Gene Description:
BCL2 like 11
Target Gene Accession:
NM_138621.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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 protein encoded by this gene contains a Bcl-2 homology domain 3 (BH3). It has been shown to interact with other members of the BCL-2 protein family, including BCL2, BCL2L1/BCL-X(L), and MCL1, and to act as an apoptotic activator. The expression of this gene can be induced by nerve growth factor (NGF), as well as by the forkhead transcription factor FKHR-L1, which suggests a role of this gene in neuronal and lymphocyte apoptosis. Transgenic studies of the mouse counterpart suggested that this gene functions as an essential initiator of apoptosis in thymocyte-negative selection. Several alternatively spliced transcript variants of this gene have been identified.
Gene References into function
- Functional study of the mouse homolog
- Identification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosis.
- direct addition of BimL to mitochondria does not lead to cytochrome c release
- Bim has an ability to activate directly the voltage-dependent anion channel, which plays an important role in apoptosis of mammalian cells.
- BimEL activate Bax by damaging the mitochondrial membrane structure directly, in addition to its binding and antagonizing Bcl-2/Bcl-XL function.
- BIM has a role in facilitating HIV-1 tat-induced apoptosis
- Data show that detachment-induced expression of Bim requires a lack of beta(1)-integrin engagement, downregulation of EGF receptor (EGFR) expression and inhibition of Erk signalling.
- Bim mRNA and protein levels increase after up-regulation of FoxO3a by paclitaxel, causing apoptosis in breast cancer cells
- phosphorylation of Bim-EL by Erk1/2 on serine 69 selectively leads to its proteasomal degradation and therefore represents a new and important mechanism of Bim regulation
- The proapoptotic effect of BIM (through transcriptional induction of two of its isoforms)is inhibited by the activation of Raf/ERK signalling which prevents BIM up-regulation and leads to phosphorylation of the BimEL isoform.
- new insights into the post-translational regulation of Bim(EL)
- Bim(EL) can be activated downstream of the caspase cascade, leading to a positive feedback amplification of apoptotic signals.
- A new pathway for Bim regulation is based on extracellular signal-regulated kinase-dependent phosphorylation of the BimEL isoform and proteasome-ddependent degradation of BimEL, followed by increased expression of shorter apoptotic isoforms BimL and BimS
- Immunosuppressive agents block Bim up-regulation and rescue T cells from death receptor-independent cell death.
- Bim appears to be a key event in cAMP-promoted apoptosis in both murine and human T-cell lymphoma and leukemia cells and thus appears to be a convergence point for the killing of such cells by glucocorticoids and agents that elevate cAMP.
- Mcl-1L degradation by either GrB or caspase-3 interferes with Bim sequestration by Mcl-1L
- Lovastatin-induced cell death occurs in correlation with significantly increased levels of the BH3-only protein, Bim in susceptible glioblastoma cell lines; up-regulation of Bim was directly associated with increased incidence of apoptosis
- expression pattern of Bim isoforms shows tissue specificity; the BH3 domain is sufficiency for proapoptotic activity; the functional state of Bims might be regulated both in the transcript and post transcript process
- Cleavage of Mcl-1 by caspases modifies its subcellular localization, increases its association with Bim and inhibits its antiapoptotic function.
- In myeloma cells, Mcl-1 neutralizes Bim through complex formation and therefore prevents apoptosis.
- BimEL is an important determinant for induction of anoikis sensitivity by mitogen-activated protein/extracellular signal-regulated kinase kinase inhibitors
- the induction of Bim by GC is a required event for the complete apoptotic response in pre-B ALL cells
- T cell blasts surviving activation-induced cell deathare memory CD44 high cells with increased BIM expression.
- activation of transcription is activated by FoxO3A
- Bim is a critical molecular link between the microtubule poison, paclitaxel, and apoptosis.
- The region unique to BimEL (amino acids 41-97, exon 3) accounts for ERK1/2 binding, ERK1/2-dependent phosphorylation, and turnover of BimEL.
- degraded during Chlamydia trachomatis infection
- degraded in Chlamydia trachomatis-infected cells
- Bik and Bim have roles in bortezomib sensitization of cells to killing by death receptor ligand TRAIL
- results show that Forkhead transcription factor 4-dependent expression of Bim protein plays a pivotal role for endothelial progenitor cell apoptosis
- expression of Bim is increased by zinc pyrithione, which induces apoptosis
- Bim is a critical regulator of luminal apoptosis during mammary acinar morphogenesis in vitro and may be an important target of oncogenes that disrupt glandular epithelial architecture.
- identified the transcriptional initiation site and three candidate remote enhancer/silencer regions of the Bim gene. However, none of these transcriptional regulatory elements was IL-3-dependent
- Repression of BIM is favored in human glioblastoma.
- Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of MCL1 and BIM and a decrease in the MCL1/BIM complex.
- Bax, Bad, and Bim are upregulated, while Bcl-2 is downregulated in human neuroblastoma cells treated with propargylamine
- The muscarinic receptor-protein kinase C signaling pathway is a regulator of Bim in neuroblastoma cells; activation of muscarinic receptors and protein kinase C o induces Bim phosphorylation, followed by down-regulation of this proapoptotic protein.
- TGF-beta is involved in the physiological loss of gastric epithelial cells by activating apoptosis mediated by Smad7, Bim, and caspase-9
- Ser(87) of Bim(EL) is an important regulatory site that is targeted by Akt to attenuate the pro-apoptotic function of Bim(EL), thereby promoting cell survival
- RUNX3 cooperates with FoxO3a/FKHRL1 to participate in the induction of apoptosis by activating Bim
- concomitant induction of E2F1 targets ASK1 and Bim by HDACIs warrants an effective activation of E2F1-dependent apoptosis in response to suberoylanilide hydroxamic acid
- Mcl-1 may serve as a direct substrate for TRAIL-activated caspases implying the existence of a novel TRAIL/caspase-8/Mcl-1/Bim communication mechanism between the extrinsic and the intrinsic apoptotic pathways
- Ceramide induces apoptosis of human colon carcinoma HT-29 cells by affecting the expression of Bcl-2 family gene members and impacting the mitochondrial function.
- Radiation therapy for squamous cell carcinoma of cervix results in increased apoptosis with the up-regulation of Bax, a proapoptotic protein, the down-regulation of Bcl-XL, an antiapoptotic protein, and no significant change in the levels of Bcl-2.
- We conclude that Noxa and Bim establish a connection between FKHRL1 and mitochondria, and that both BH3-only proteins are critically involved in FKHRL1-induced apoptosis in neuroblastoma.
- These results suggest that the high expression of cell adhesion-related proteins might be responsible for the different apoptosis status after the transfection of Bim L.
- Bim plays an essential role in synergistic induction of apoptosis by SBHA and TRAIL in melanoma.
- The main pathway by which Fas signaling regulates the levels of Bim expression in human T-cell blasts is the death-domain- and caspase-independent generation of discrete levels of H2O2, which results in the net increase of Foxo3a levels.
- Inhibition of endogenously produced IGFBP-5 is associated with Bim-dependent apoptosis in NB cells.
- in addition to interacting with the pro-apoptotic protein Bak, vaccinia F1L also functions to indirectly inhibit the activation of Bax, likely by interfering with the pro-apoptotic activity of BH3-only proteins such as BimL
- TLR stimulation of macrophages can regulate Bim levels in opposing ways, namely by transcriptional induction and by phosphorylation-dependent degradation of the protein.
- results implicate BIM in glucocorticoid-induced apoptosis in chronic lymphocytic leukemia cells through proteasome degradation.
- results indicate that IFN-alpha causes apoptosis in myeloma cells through a moderate triggering of the mitochondrial route initiated by Bim
- Our results confirm that ultrasound induces apoptosis via a pathway that involves Bak, Bcl-2, and caspases, but not ROS.
- Bax and Bim are upregulated in human B cells during arsenic trioxide induction of apoptosis via the mitochondrial pathway
- A cytokine-mediated posttranscriptional regulation of Bim mRNA by heat-shock cognate protein 70 (Hsc70), which binds to AU-rich elements (AREs) in the 3'-untranslated region of specific mRNAs and enhances their stability, is presented.
- Bim is an essential mediator of amyloid-beta-induced neurotoxicity.
- These data provide important mechanistic information on the processes involved in sculpting the mammary gland and demonstrate that BIM is a critical regulator of apoptosis in vivo.
- results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak
- Loss of expression of the pro-apoptotic protein Bim is associated with renal cell carcinoma
- These results demonstrate that BimL is involved in UV irradiation-induced apoptosis by indirectly activating Bax.
- preformed Bim(EL)/Mcl-1 and Bim(EL)/Bcl-x(L) complexes can be rapidly dissociated following activation of ERK1/2 by survival factors
- FXa plays a key role in cellular processes in which Bim is the central player in determining cell survival.
- a Bim-dependant pathway modulated by cytokines is involved in apoptosis of chronic myeloid leukemia cells induced by imatinib and nilotinib
- Bim loss may play an important role in melanoma progression
- In the absence of Bim, EBNA3A and EBNA3C appear to provide no survival advantage in Burkitt's lymphoma cells.
- TRAIL can trigger an apoptotic pathway that involves JNK-dependent activation of Bim, which in turn induces Bax-mediated permeabilization of lysosomes.
- Mcl-1 confers TRAIL resistance by serving as a buffer for Bak, Bim, and Puma, and sorafenib is a potential modulator of TRAIL sensitivity
- Bim mediates particulate matter-induced apoptosis via mitochondrial pathway.
- The open reading frame of BimSs3 may initiate at the second ATG and encodes a 36 amino-acid peptide with BH3 domain.
- Mcl-1 degradation primes the cell for Bim and Bax activation and anoikis, which can be blocked by oncogenic signaling in metastatic cells
- PINCH-1 contributes to apoptosis resistance through suppression of Bim. Mechanistically, PINCH-1 suppresses Bim not only transcriptionally but also post-transcriptionally.
- Bim is a novel regulator of osteoblast apoptosis and may be a therapeutic target.
- BIM is induced by lung cancer cell lines that are sensitive to erlotinib but not by those resistant.
- In the absence of serum, the suppression of either Bad, Bim or Bid expression delayed cell death under several stress conditions
- In addition to its proapoptotic effect, IL-21 promoted STAT1 and STAT5 phosphorylation in natural killer cells with concurrent enhanced antibody-dependent cellular cytotoxicity against rituximab-coated CLL cells
- BIM and tBID follow different strategies to trigger BAX-driven mitochondrial outer membrane permeabilization with strong potency
- Bad and Bim are major B-RAF responsive proteins regulating apoptosis in melanoma cells.
- data indicate that Bim, Bak, and Bax actively mediate osteoblast apoptosis induced by trophic factor withdrawal
- Bim-mediated apoptosis following actin damage due to deregulation of Cdk2 and the cell cycle by the absence of functional p53.
- variations in c-myc and p21(WAF1) expression delay apoptosis making PBL resistant to sodium butyrate for several hours
- arsenic trioxide upregulated expression of Bmf, Noxa, and Bim. Silencing of Bmf, Noxa, and Bim significantly protected MM cells from ATO-induced apoptosis
- Activated extracellular signal-regulated kinase in epithelial cells infected with N. gonorrheae targeted Bad and Bim for downregulation at the protein level.
- Data suggest that Bim-mediated attrition of HBV-specific CD8(+) T cells contributes to the inability of these cell populations to persist and control viral replication.
- ABT-737 augments TRAIL-induced cell killing by unsequestering Bim and Bak and enhancing a Bax conformational change induced by TRAIL.
- RACK1 has a role in protecting cancer cells from apoptosis by regulating the degradation of BimEL, which together with CIS could play an important role of drug resistance in chemotherapy
- B-Raf-initiated inactivation of Bad and Bim only partly contributes to the anti-apoptotic activities of this oncogene and that other points within the cell death machinery are also targeted by deregulated ERK signaling
- The identification of a novel putative human BCL2L11 promoter provides new insights into the structure and regulation of the BCL2L11 locus.
- These findings suggest JNK to have an important pro-apoptotic function following ultraviolet rays B irradiation in human melanocytes, by acting upstream of lysosomal membrane permeabilization and Bim phosphorylation.
- N-RAS(Q61K) and B-RAF(V600E) contribute to melanoma's resistance to apoptosis in part by downregulating Bim expression
- Endogenous MIF may regulate the pro-apoptotic activity of Bim and inhibit the release of cytochrome c from mitochondria.
- These data suggest that regulation of BIM expression by BRAF-->MEK-->ERK signaling is one mechanism by which oncogenic BRAF(V600E) can influence the aberrant physiology of melanoma cells.
- BIM plays a significant role in T cell receptor (TCR)-induced death of activated human T cells, working in tandem with FAS signaling as a separate signal to kill T cells.
- study concludes a single endogenous BRAF(V600E) allele is sufficient to repress BIM & prevent death from growth factor withdrawal; colorectal cancer cells with V600E mutations are addicted to the ERK1/2 pathway for repression of BIM
- The crystal structure of Bfl-1, the last anti-apoptotic Bcl-2 family member to be structurally characterized, in complex with a peptide corresponding to the BH3 region of the pro-apoptotic protein Bim is presented.
- Treatment of B-RAF mutant tumor cells with a MEK inhibitor requires BIM and is enhanced by a BH3 mimetic.
- Scleroderma serum-induced EPC apoptosis is mediated chiefly by the Akt-FOXO3a-Bim pathway, which may account, at least in part, for the decreased circulating EPC levels in scleroderma patients.
- A proapoptotic signaling pathway involving RasGRP, Erk, and Bim in B cells
- Bim is not absolutely required for paclitaxel cytotoxicity in breast cancer cell lines.
- betaTrCP promotes cell survival in cooperation with the ERK-RSK pathway by targeting BimEL for degradation.