Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation by the MGI curatorial staff, curated orthology
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
The bcl-2 knockout mouse exhibits marked changes in osteoblast phenotype and collagen deposition in bone as well as a mild growth plate phenotype.
Alterations in cell death and cell cycle progression in the UV-irradiated epidermis of bcl-2-deficient mice.
Retinal ganglion cell loss after the period of naturally occurring cell death in bcl-2-/- mice.
Targeted disruption of the bcl-2 gene in mice exacerbates focal ischemic brain injury.
Bax and Bcl-2 interaction in a transgenic mouse model of familial amyotrophic lateral sclerosis.
Bis, a Bcl-2-binding protein that synergizes with Bcl-2 in preventing cell death.
Damage-induced apoptosis in intestinal epithelia from bcl-2-null and bax-null mice: investigations of the mechanistic determinants of epithelial apoptosis in vivo.
Hair follicle apoptosis and Bcl-2.
Developmental changes in antioxidant enzymes and oxidative damage in kidneys, liver and brain of bcl-2 knockout mice.
Differences in bcl-2- and bax-independent function in regulating apoptosis in sensory neuron populations.
Effects of deficiency in p53 or bcl-2 on the sensitivity of clonogenic cells in the small intestine to low dose-rate irradiation.
Patterns of cell death in mouse anteroventral cochlear nucleus neurons after unilateral cochlea removal.
Pro- and anti-apoptotic members of the Bcl-2 family in skeletal muscle: a distinct role for Bcl-2 in later stages of myogenesis.
Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.
Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis.
Degenerative disorders caused by Bcl-2 deficiency prevented by loss of its BH3-only antagonist Bim.
Intrinsic and extrinsic pathway signaling during neuronal apoptosis: lessons from the analysis of mutant mice.
bcl-2 overexpression promotes myocyte proliferation.
A novel transactivating factor that regulates interferon-gamma-dependent gene expression.
Proapoptotic activity of ITM2B(s), a BH3-only protein induced upon IL-2-deprivation which interacts with Bcl-2.
Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viability.
Sorting specificity of spermatogenic cell specific region of mouse hexokinase-s (mHk1-s).
Calcium-dependent interaction of calcineurin with Bcl-2 in neuronal tissue.
Bcl2 retards G1/S cell cycle transition by regulating intracellular ROS.
Bcl-2 confers growth and survival advantage to interleukin 7-dependent early pre-B cells which become factor independent by a multistep process in culture.
Targeted disruption of the PDZK1 gene in mice causes tissue-specific depletion of the high density lipoprotein receptor scavenger receptor class B type I and altered lipoprotein metabolism.
Integrated analysis of protein composition, tissue diversity, and gene regulation in mouse mitochondria.
Mono- and multisite phosphorylation enhances Bcl2's antiapoptotic function and inhibition of cell cycle entry functions.
Interaction of bcl-2 with Paxillin through its BH4 domain is important during ureteric bud branching.
TCR-independent and caspase-independent apoptosis of murine thymocytes by CD24 cross-linking.
Alterations in cell-adhesive and migratory properties of proximal tubule and collecting duct cells from bcl-2 -/- mice.
Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum.
Proapoptotic BAX and BAK control multiple initiator caspases.
Polycystic kidney disease prevented by transgenic RNA interference.
Frag1, a homolog of alternative replication factor C subunits, links replication stress surveillance with apoptosis.
Increased anxiety-like behaviors and mitochondrial dysfunction in mice with targeted mutation of the Bcl-2 gene: further support for the involvement of mitochondrial function in anxiety disorders.
Loss of PKD1 and loss of Bcl-2 elicit polycystic kidney disease through distinct mechanisms.
Indispensable role of Bcl2 in the development of the melanocyte stem cell.
IAN family critically regulates survival and development of T lymphocytes.
Suppression of ureteric bud apoptosis rescues nephron endowment and adult renal function in Pax2 mutant mice.
PP2A regulates BCL-2 phosphorylation and proteasome-mediated degradation at the endoplasmic reticulum.
Mitochondrial rhomboid PARL regulates cytochrome c release during apoptosis via OPA1-dependent cristae remodeling.
Role of Bcl-2 expression for productive herpes simplex virus 2 replication.
Radiation-induced gastric epithelial apoptosis occurs in the proliferative zone and is regulated by p53, bak, bax, and bcl-2.
Regulation of the lifespan in dendritic cell subsets.
c-Myc is essential for urokinase plasminogen activator expression on hypoxia-induced vascular smooth muscle cells.
Involvement of heat shock protein (Hsp)90 beta but not Hsp90 alpha in antiapoptotic effect of CpG-B oligodeoxynucleotide.
Bim/Bcl-2 balance is critical for maintaining naive and memory T cell homeostasis.
Dual role of proapoptotic BAD in insulin secretion and beta cell survival.
Osteoclast size is controlled by Fra-2 through LIF/LIF-receptor signalling and hypoxia.
A mitochondrial protein compendium elucidates complex I disease biology.
Upregulation of Bcl2 inhibits apoptosis-driven BAX insertion but favors BAX relocalization in mitochondria.
Endogenous HMGB1 regulates autophagy.
Cyclic-AMP-dependent protein kinase A regulates apoptosis by stabilizing the BH3-only protein Bim.
Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis.
Deacetylation of p53 induces autophagy by suppressing Bmf expression.
BOK Is a Non-canonical BCL-2 Family Effector of Apoptosis Regulated by ER-Associated Degradation.
Degradation of Bcl-2 by XIAP and ARTS Promotes Apoptosis.
Disruption of the beclin 1-BCL2 autophagy regulatory complex promotes longevity in mice.
Exercise-activated hepatic autophagy via the FN1-α5β1 integrin pathway drives metabolic benefits of exercise.
Bcl-2 overexpression prevents motoneuron cell body loss but not axonal degeneration in a mouse model of a neurodegenerative disease.
Role of BCL-2 in the survival and function of developing and mature sympathetic neurons.
Differential regulation of bcl-2, bax, c-fos, junB, and krox-24 expression in the cerebellum of Purkinje cell degeneration mutant mice.
Bcl-2 protects neural cells from cyanide/aglycemia-induced lipid oxidation, mitochondrial injury, and loss of viability.
Ablation of bcl-2 gene expression decreases the numbers of oocytes and primordial follicles established in the post-natal female mouse gonad.
Expression of Bcl-2, Bcl-x, and Bax after T cell activation and IL-2 withdrawal.
Bcl-XL and Bcl-2 repress a common pathway of cell death.
Up-regulation of bax and down-regulation of bcl-2 is associated with kainate-induced apoptosis in mouse brain.
Apoptosis and Bcl-2 expression in cultured murine splenic T cells.
Evolutionary conservation of function among mammalian, avian, and viral homologs of the Bcl-2 oncoprotein.
bcl-2 deficiency in mice leads to pleiotropic abnormalities: accelerated lymphoid cell death in thymus and spleen, polycystic kidney, hair hypopigmentation, and distorted small intestine.
Cloning and functional analysis of BAG-1: a novel Bcl-2-binding protein with anti-cell death activity.
Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death.
Fulminant metanephric apoptosis and abnormal kidney development in bcl-2-deficient mice.
The intracellular distribution and pattern of expression of Mcl-1 overlap with, but are not identical to, those of Bcl-2.
Bcl-2 overexpression abolishes early calcium waving preceding apoptosis in NIH-3T3 murine fibroblasts.
Expression of Bcl-2 protein in murine neural cells in culture.
Evidence that BCL-2 represses apoptosis by regulating endoplasmic reticulum-associated Ca2+ fluxes.
Bcl-2 protein expression during murine development.
bcl-2 gene prevents apoptosis of basic fibroblast growth factor-deprived murine aortic endothelial cells.
bcl-2 gene enables rescue from in vitro myelosuppression (bone marrow cell death) induced by chemotherapy.
Antisense oligonucleotides suppress B-cell lymphoma growth in a SCID-hu mouse model.
Targeted disruption of Bcl-2 alpha beta in mice: occurrence of gray hair, polycystic kidney disease, and lymphocytopenia.
Developmental regulation of the Bcl-2 protein and susceptibility to cell death in B lymphocytes.
Disappearance of the lymphoid system in Bcl-2 homozygous mutant chimeric mice.
Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair.
Apoptosis during an early stage of nephrogenesis induces renal hypoplasia in bcl-2-deficient mice.
Bax promotes neuronal survival and antagonises the survival effects of neurotrophic factors.
Diminished cell proliferation associated with the death-protective activity of Bcl-2.
Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development.
Accelerated disappearance of melanocytes in bcl-2-deficient mice.
Abnormal postpartum renal development and cystogenesis in the bcl-2 (-/-) mouse.
Distinct patterns of Fas cell surface expression during development of T- or B-lymphocyte lineages in normal, scid, and mutant mice lacking or overexpressing p53, bcl-2, or rag-2 genes.
BID: a novel BH3 domain-only death agonist.
Bcl-2 prevents hippocampal cell death induced by the neuroleptic drug haloperidol.
Bcl-2 lies downstream of parathyroid hormone-related peptide in a signaling pathway that regulates chondrocyte maturation during skeletal development.
Bcl-2 promotes regeneration of severed axons in mammalian CNS.
Role of bcl-2 in the development of lymphoid cells from the hematopoietic stem cell.
Valproic acid-induced changes in gene expression during neurulation in a mouse model.
Susceptibility of cerebellar granule neurons derived from Bcl-2-deficient and transgenic mice to cell death.
The apoptosis and proliferation of SAC-activated B cells by IL-10 are associated with changes in Bcl-2, Bcl-xL, and Mcl-1 expression.
Differential involvement of caspases in apoptosis of myeloid leukemic cells induced by chemotherapy versus growth factor withdrawal.
Bcl-2 can rescue T lymphocyte development in interleukin-7 receptor-deficient mice but not in mutant rag-1-/- mice.
Bcl-2 and Bax function independently to regulate cell death.
Bcl-2 is required for cranial sensory neuron survival at defined stages of embryonic development.
Bcl-2 accelerates the maturation of early sensory neurons.
Bax directly induces release of cytochrome c from isolated mitochondria.
Enhanced oxidative stress and altered antioxidants in brains of Bcl-2-deficient mice.
Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria.
Nuclear localization of beta-catenin and loss of apical brush border actin in cystic tubules of bcl-2 -/- mice.
UniProt record for mouse Bcl2
Bioreason deep research report on mouse Bcl2
Falcon deep research report on mouse Bcl2
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The report summarizes the conserved BH3-binding antiapoptotic mechanism; much of its recent evidence concerns human BCL2, so mouse-specific primary studies are evaluated separately.
"Mechanistically, BCL-2 binds BH3-containing partners through its groove, thereby preventing downstream **BAX/BAK oligomerization** and **pore formation** in the mitochondrial outer membrane that would otherwise cause **MOMP** and apoptosis."
Channel formation by antiapoptotic protein Bcl-2.
Bcl-2 is located predominantly in the inner membrane and crista of mitochondria in rat liver.
Iron induces Bcl-2 expression in human dermal microvascular endothelial cells.
A functional role for nicotine in Bcl2 phosphorylation and suppression of apoptosis.
The HIV-1 viral protein R induces apoptosis via a direct effect on the mitochondrial permeability transition pore.
Manual primary source checks for Bcl2 modification and DNA-binding annotations
OpenScientist BCL2 conditional proapoptotic and channel-capacity adjudication
A short Nur77-derived peptide converts Bcl-2 from a protector to a killer.
During negative selection, Nur77 family proteins translocate to mitochondria where they associate with Bcl-2 and expose its proapoptotic BH3 domain.
T cell-specific inhibition of multiple apoptotic pathways blocks negative selection and causes autoimmunity.