HCSGD entry for BCL2L1
1. General information
| Official gene symbol | BCL2L1 |
|---|---|
| Entrez ID | 598 |
| Gene full name | BCL2-like 1 |
| Other gene symbols | BCL-XL/S BCL2L BCLX BCLXL BCLXS Bcl-X PPP1R52 bcl-xL bcl-xS |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000910 | Cytokinesis | IMP | biological_process |
| GO:0001541 | Ovarian follicle development | IEA | biological_process |
| GO:0001701 | In utero embryonic development | IEA | biological_process |
| GO:0001836 | Release of cytochrome c from mitochondria | IDA IEA | biological_process |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0005739 | Mitochondrion | IDA | cellular_component |
| GO:0005741 | Mitochondrial outer membrane | IDA NAS TAS | cellular_component |
| GO:0005743 | Mitochondrial inner membrane | IEA | cellular_component |
| GO:0005759 | Mitochondrial matrix | IEA | cellular_component |
| GO:0005813 | Centrosome | IDA | cellular_component |
| GO:0005829 | Cytosol | IEA | cellular_component |
| GO:0006897 | Endocytosis | IEA | biological_process |
| GO:0006915 | Apoptotic process | TAS | biological_process |
| GO:0007093 | Mitotic cell cycle checkpoint | IMP | biological_process |
| GO:0007281 | Germ cell development | IEA | biological_process |
| GO:0007283 | Spermatogenesis | IEA | biological_process |
| GO:0008283 | Cell proliferation | IEA | biological_process |
| GO:0008284 | Positive regulation of cell proliferation | IEA | biological_process |
| GO:0008584 | Male gonad development | IEA | biological_process |
| GO:0008630 | Intrinsic apoptotic signaling pathway in response to DNA damage | IEA | biological_process |
| GO:0008637 | Apoptotic mitochondrial changes | TAS | biological_process |
| GO:0009566 | Fertilization | IEA | biological_process |
| GO:0010507 | Negative regulation of autophagy | TAS | biological_process |
| GO:0016021 | Integral component of membrane | IEA | cellular_component |
| GO:0019050 | Suppression by virus of host apoptotic process | IDA | biological_process |
| GO:0019901 | Protein kinase binding | IPI | molecular_function |
| GO:0030054 | Cell junction | IEA | cellular_component |
| GO:0030672 | Synaptic vesicle membrane | IEA | cellular_component |
| GO:0031965 | Nuclear membrane | IEA | cellular_component |
| GO:0031966 | Mitochondrial membrane | IEA | cellular_component |
| GO:0034097 | Response to cytokine | IDA | biological_process |
| GO:0035872 | Nucleotide-binding domain, leucine rich repeat containing receptor signaling pathway | TAS | biological_process |
| GO:0040007 | Growth | IEA | biological_process |
| GO:0042802 | Identical protein binding | IPI | molecular_function |
| GO:0042803 | Protein homodimerization activity | IBA | molecular_function |
| GO:0043065 | Positive regulation of apoptotic process | IEA | biological_process |
| GO:0043066 | Negative regulation of apoptotic process | IDA IMP | biological_process |
| GO:0043524 | Negative regulation of neuron apoptotic process | IEA | biological_process |
| GO:0045087 | Innate immune response | TAS | biological_process |
| GO:0046898 | Response to cycloheximide | IEA | biological_process |
| GO:0046902 | Regulation of mitochondrial membrane permeability | IDA | biological_process |
| GO:0046982 | Protein heterodimerization activity | IBA IEA | molecular_function |
| GO:0051402 | Neuron apoptotic process | IEA | biological_process |
| GO:0051434 | BH3 domain binding | IPI | molecular_function |
| GO:0051881 | Regulation of mitochondrial membrane potential | IDA | biological_process |
| GO:0060154 | Cellular process regulating host cell cycle in response to virus | IEA | biological_process |
| GO:0071230 | Cellular response to amino acid stimulus | IEA | biological_process |
| GO:0071312 | Cellular response to alkaloid | IEA | biological_process |
| GO:0071480 | Cellular response to gamma radiation | IEA | biological_process |
| GO:0071839 | Apoptotic process in bone marrow | IEA | biological_process |
| GO:0090005 | Negative regulation of establishment of protein localization to plasma membrane | IDA | biological_process |
| GO:0090201 | Negative regulation of release of cytochrome c from mitochondria | IC IDA | biological_process |
| GO:0097136 | Bcl-2 family protein complex | IDA | cellular_component |
| GO:0097192 | Extrinsic apoptotic signaling pathway in absence of ligand | IBA IEA | biological_process |
| GO:0097193 | Intrinsic apoptotic signaling pathway | TAS | biological_process |
| GO:0097284 | Hepatocyte apoptotic process | IEA | biological_process |
| GO:1900118 | Negative regulation of execution phase of apoptosis | IDA | biological_process |
| GO:1902230 | Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage | IDA | biological_process |
| GO:2000811 | Negative regulation of anoikis | IMP | biological_process |
| GO:2001240 | Negative regulation of extrinsic apoptotic signaling pathway in absence of ligand | TAS | biological_process |
| GO:2001243 | Negative regulation of intrinsic apoptotic signaling pathway | IDA | biological_process |
| GO:2001244 | Positive regulation of intrinsic apoptotic signaling pathway | TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0043665324 | 0.9960248851 | 0.1760215926 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Up | 0.3330583485 |
| GSE13712_SHEAR | Up | 0.9304838495 |
| GSE13712_STATIC | Up | 0.5209951213 |
| GSE19018 | Up | 0.0841309333 |
| GSE19899_A1 | Up | 0.1913026629 |
| GSE19899_A2 | Up | 1.0507354884 |
| PubMed_21979375_A1 | Up | 0.2669526696 |
| PubMed_21979375_A2 | Up | 0.5612190100 |
| GSE35957 | Up | 0.6712826595 |
| GSE36640 | Up | 0.6274105225 |
| GSE54402 | Up | 0.3781071297 |
| GSE9593 | Up | 1.3697820903 |
| GSE43922 | Up | 0.1341153022 |
| GSE24585 | Up | 0.0681976079 |
| GSE37065 | Up | 0.0810582438 |
| GSE28863_A1 | Down | -0.0195148749 |
| GSE28863_A2 | Up | 0.0750003165 |
| GSE28863_A3 | Up | 0.0822232800 |
| GSE28863_A4 | Up | 0.1767659871 |
| GSE48662 | Up | 0.2994642869 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| 4'-FLUORO-1,1'-BIPHENYL-4-CARBOXYLIC ACID | DB07108 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-491-5p | MIMAT0002807 | MIRT004285 | Luciferase reporter assay//Western blot | Functional MTI | 20039318 |
| hsa-let-7g-5p | MIMAT0000414 | MIRT004490 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20347499 |
| hsa-let-7c-5p | MIMAT0000064 | MIRT004491 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20347499 |
| hsa-miR-122-5p | MIMAT0000421 | MIRT023334 | Western blot;qRT-PCR | Non-Functional MTI | 18692484 |
| hsa-miR-30a-5p | MIMAT0000087 | MIRT028457 | Proteomics | Functional MTI (Weak) | 18668040 |
| hsa-miR-484 | MIMAT0002174 | MIRT042070 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-23b-3p | MIMAT0000418 | MIRT046292 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-133a-3p | MIMAT0000427 | MIRT052647 | Luciferase reporter assay//Western blot | Functional MTI | 23756231 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 14 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27398719 | Dynamic Bcl-xL (S49) and (S62) Phosphorylation/Dephosphorylation during Mitosis Prevents Chromosome Instability and Aneuploidy in Normal Human Diploid Fibroblasts |
| 27398719 | Bcl-xL proteins undergo dynamic phosphorylation/dephosphorylation on Ser49 and Ser62 residues during mitosis |
| 27398719 | We studied normal human diploid BJ foreskin fibroblast cells expressing Bcl-xL (wild type), (S49A), (S49D), (S62A), (S62D) and the dual-site (S49/62A) and (S49/62D) mutants |
| 27398719 | Fluorescence in situ hybridization analysis and Giemsa-banded karyotypes revealed that the expression of Bcl-xL phosphorylation mutants in normal diploid BJ cells provoked chromosome instability and aneuploidy |
| 27398719 | They could impact future strategies aiming to develop and identify compounds that could target not only the anti-apoptotic domain of Bcl-xL protein, but also its mitotic domain for cancer therapy |
| 27048913 | Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL |
| 27048913 | Here we show that senescent cells upregulate the anti-apoptotic proteins BCL-W and BCL-XL |
| 27048913 | Joint inhibition of BCL-W and BCL-XL by siRNAs or the small-molecule ABT-737 specifically induces apoptosis in senescent cells |
| 26711051 | Among other pro-survival regulators identified was Bcl-xl |
| 26711051 | Like D and Q, N is senolytic in some, but not all types of senescent cells: N reduced viability of senescent human umbilical vein epithelial cells (HUVECs), IMR90 human lung fibroblasts, and murine embryonic fibroblasts (MEFs), but not human primary preadipocytes, consistent with our previous finding that Bcl-xl siRNA is senolytic in HUVECs, but not preadipocytes |
| 26711051 | N targets Bcl-2, Bcl-xl, and Bcl-w, while T targets Bcl-2, Bcl-xl, and Mcl-1 |
| 26711051 | The combination of Bcl-2, Bcl-xl, and Bcl-w siRNAs was senolytic in HUVECs and IMR90 cells, while combination of Bcl-2, Bcl-xl, and Mcl-1 siRNAs was not |
| 26657143 | To test this idea, we screened a collection of compounds and identified ABT263 (a specific inhibitor of the anti-apoptotic proteins BCL-2 and BCL-xL) as a potent senolytic drug |
| 25882843 | Alternately, Mito-Pim1 enhances survival by increasing expression of Bcl-2 and Bcl-XL and decreasing cell death after H2O2 treatment, thereby preserving mitochondrial integrity superior to PimWT |
| 25754370 | Using siRNA to silence expression of key nodes of this network, including ephrins (EFNB1 or 3), PI3Kdelta, p21, BCL-xL, or plasminogen-activated inhibitor-2, killed senescent cells, but not proliferating or quiescent, differentiated cells |
| 24484372 | HCT116 cells, which upregulated both pro-apoptotic Bax and anti-apoptotic Bcl-xL in the early response to melatonin treatment, activated autophagic as well as apoptotic machinery within 18 hr |
| 24055032 | Clinical significance of proliferation, apoptosis and senescence of nasopharyngeal cells by the simultaneously blocking EGF, IGF-1 receptors and Bcl-xl genes |
| 24055032 | METHOD: We have constructed multiple shRNA expression vectors of targeting EGFR, IGF1R and Bcl-xl, which were transfected to the CNE2 cells |
| 24055032 | The growth of the cells, cell cycle progression, apoptosis of the cells, senescent tumor cells and the proteins of EGFR, IGF1R and Bcl-xl were analyzed by MTT, flow cytometry, cytochemical therapy or Western blot |
| 24055032 | RESULTS: In group of simultaneously blocking EGFR, IGF1R and Bcl-xl genes, the mRNA of EGFR, IGF1R and Bcl-xl expression was decreased by (66 |
| 24055032 | CONCLUSIONS: Simultaneously blocking EGFR, IGF1R and Bcl-xl genes is capable of altering the balance between proliferating versus apoptotic and senescent cells in the favor of both of apoptosis and senescence and, therefore, the tumor cells regression |
| 21212468 | Remarkably, overexpressed Zfra induces apoptosis via the mitochondrial pathway, which involves suppression of Bcl-2 and Bcl-xL expression (without causing cytochrome c release), counteracting the apoptotic function of tumor suppressor p53 and WWOX, and dissipation of mitochondrial membrane potential for ultimately leading to cell death |
| 18262222 | Progressive apoptosis resistance prior to senescence and control by the anti-apoptotic protein BCL-xL |
| 18262222 | In young cells, the level of anti-apoptotic protein BCL-xL quickly fell after UV irradiation while pro-apoptotic protein BAX rose |
| 18262222 | Instead of decreasing, the level of BCL-xL increased dramatically after UV stress so that the ratio of pro-apoptotic BAX to anti-apoptotic BCL-xL remained low |
| 18262222 | RNAi against BCL-xL restored the UV-sensitivity of old cells, indicating that BCL-xL is itself responsible for the pre-senescence decline in the ability of a genotoxic stress to induce apoptosis |
| 15922292 | The antiapoptotic Bcl-2 family proteins Bcl-2 and Bcl-xL play important roles in inhibiting mitochondria-dependent extrinsic and intrinsic cell death pathways |
| 15922292 | The overexpression of Bcl-2 may also have the ability to enhance cell death in the interaction of Bcl-xL with other factors |
| 15922292 | The overexpression of Bcl-xL enhances autophagic cell death when apoptotic cell death is inhibited in Bax(-/-)/Bak(-/-) double knockout cells |
| 15922292 | This review discusses the previously unexplained aspects of Bcl-2 and Bcl-xL functions associated with cell death, for better understanding of their functions in the regulation |
| 15520191 | To understand which JNK-mediated pathway may be involved, a number of JNK target proteins were examined, including the transcription factor, c-Jun, and the apoptotic regulatory proteins Bcl-X(L) and Bim |
| 15520191 | Ceramide did not promote Bcl-X(L) phosphorylation |
| 14653227 | Pro-death Bax increased, while anti-death Bcl-2 and Bcl-XL decreased, and apoptotic TUNEL-positive cells were detected in the hippocampus of klotho mutant mice at the age of 7 weeks |
| 12473065 | Similarities between preparations included: an enhanced ability for both Apo2L/TRAIL preparations to kill a greater relative percentage of HaCaT cells compared with keratinocytes; enhanced cytotoxicity towards keratinocytes that had their NF-B activity inhibited; a dependence of both Apo2L/TRAIL preparations on FADD and caspase activation; triggering of the same caspase cascades including caspase 8 and 3; and an ability to induce apoptosis even when HaCaT cells and keratinocytes were transduced to overexpress either Bcl-2 or Bcl-x(L) (survival factors that reduce susceptibility to UV-light-induced apoptosis) |
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