BAD
Bcl2-associated agonist of cell death
Also known as: BAD_HUMAN, BBC2, BCL2L8
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q92934
- Gene
- BAD
- Ensembl
- ENSG00000002330
- Chromosome
- 11
- Canonical length
- 168 aa
- Protein class
- Cancer-related genes, Predicted intracellular proteins, RAS pathway related proteins
- Subcellular location
- Mitochondria,Mid piece,Principal piece,End piece
OverviewNCBI Gene
The protein encoded by this gene is a member of the BCL-2 family. BCL-2 family members are known to be regulators of programmed cell death. This protein positively regulates cell apoptosis by forming heterodimers with BCL-xL (B-cell lymphoma-extra large) and BCL-2, and reversing their death repressor activity. Proapoptotic activity of this protein is regulated through its phosphorylation. Protein kinases AKT and MAP kinase, as well as protein phosphatase calcineurin were found to be involved in the regulation of this protein. Alternative splicing of this gene results in two transcript variants which encode the same isoform. [provided by RefSeq, Dec 2019]
Canonical amino-acid sequenceUniProt
168 residues, UniProt reviewed canonical sequence.
>Q92934|BAD
1 MFQIPEFEPS EQEDSSSAER GLGPSPAGDG PSGSGKHHRQ APGLLWDASH QQEQPTSSSH
61 HGGAGAVEIR SRHSSYPAGT EDDEGMGEEP SPFRGRSRSA PPNLWAAQRY GRELRRMSDE
121 FVDSFKKGLP RPKSAGTATQ MRQSSSWTRV FQSWWDRNLG RGSSAPSQLocalizationUniProt · AlphaFold · HPA
Whether an antibody against BAD can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Other membrane
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.67
- Highest tissue expression
- 138 nTPM
Expression across tissuesHPA
Tissue
- cerebral cortex: 138 nTPM
- amygdala: 135 nTPM
- hippocampal formation: 127 nTPM
- midbrain: 115 nTPM
- basal ganglia: 114 nTPM
- heart muscle: 111 nTPM
Single-cell type
- esophageal apical cells: 357 nCPM
- syncytiotrophoblasts: 286 nCPM
- extravillous trophoblasts: 259 nCPM
- decidual stromal cells: 195 nCPM
- migrating cytotrophoblasts: 194 nCPM
- cytotrophoblasts: 190 nCPM
Immune cell
- eosinophil: 103 nTPM
- plasmacytoid DC: 94 nTPM
- neutrophil: 93 nTPM
- basophil: 89 nTPM
- T-reg: 72 nTPM
- classical monocyte: 70 nTPM
Brain region
- thalamus: 89 nTPM
- amygdala: 77 nTPM
- midbrain: 75 nTPM
- medulla oblongata: 75 nTPM
- hippocampal formation: 74 nTPM
- cerebral cortex: 73 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.53
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.55
- DepMap mean gene effect
- -0.15
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- apoptotic process
- ATP metabolic process
- cellular response to hypoxia
- cellular response to lipid
- cellular response to mechanical stimulus
- cellular response to nicotine
- cytokine-mediated signaling pathway
- extrinsic apoptotic signaling pathway
- extrinsic apoptotic signaling pathway in absence of ligand
- extrinsic apoptotic signaling pathway via death domain receptors
- glucose catabolic process
- glucose homeostasis
- intrinsic apoptotic signaling pathway
- intrinsic apoptotic signaling pathway in response to DNA damage
- negative regulation of apoptotic process
- pore complex assembly
- positive regulation of apoptotic process
- positive regulation of autophagy
- positive regulation of B cell differentiation
- positive regulation of epithelial cell proliferation
- positive regulation of insulin secretion
- positive regulation of insulin secretion involved in cellular response to glucose stimulus
- positive regulation of mitochondrial membrane potential
- positive regulation of proteolysis
- positive regulation of release of cytochrome c from mitochondria
- positive regulation of T cell differentiation
- positive regulation of type B pancreatic cell development
- regulation of mitochondrial membrane permeability
- release of cytochrome c from mitochondria
- type B pancreatic cell proliferation
- ADP metabolic process
- positive regulation of intrinsic apoptotic signaling pathway in response to osmotic stress
Molecular functions
- cysteine-type endopeptidase activator activity
- lipid binding
- phospholipid binding
- protein kinase binding
- protein phosphatase binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Bcl2-associated agonist of cell death
- Pro-apoptotic Bcl-2 protein, BAD
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of BAD in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads BAD as an antibody target. Whether an autoantibody or antibody against BAD could matter depends on whether native BAD is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
BAD is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label BAD as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
Loading the interactive Seroatlas protein explorer...