TAL2
T-cell acute lymphocytic leukemia protein 2
Also known as: bHLHa19, TAL2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q16559
- Gene
- TAL2
- Ensembl
- ENSG00000186051
- Chromosome
- 9
- Canonical length
- 108 aa
- Protein class
- Cancer-related genes, Disease related genes, Human disease related genes, Predicted intracellular proteins, Transcription factors
- Subcellular location
- Cytosol
OverviewNCBI Gene
This intronless gene encodes a helix-loop-helix protein. Translocations between this gene on chromosome 9 and the T-cell receptor beta-chain locus on chromosome 7 have been associated with activation of the T-cell acute lymphocytic leukemia 2 gene and T-cell acute lymphoblastic leukemia. [provided by RefSeq, Mar 2009]
Canonical amino-acid sequenceUniProt
108 residues, UniProt reviewed canonical sequence.
>Q16559|TAL2
1 MTRKIFTNTR ERWRQQNVNS AFAKLRKLIP THPPDKKLSK NETLRLAMRY INFLVKVLGE
61 QSLQQTGVAA QGNILGLFPQ GPHLPGLEDR TLLENYQVPS PGPSHHIPLocalizationUniProt · AlphaFold · HPA
Whether an antibody against TAL2 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
- Unknown
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.54
- Highest tissue expression
- 13 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 13 nTPM
- kidney: 2.8 nTPM
- tongue: 2.2 nTPM
- choroid plexus: 1.3 nTPM
- epididymis: 0.6 nTPM
- retina: 0.5 nTPM
Single-cell type
- müller glia: 3.2 nCPM
- myonuclei: 2.8 nCPM
- b-cells: 2 nCPM
- other brain neurons: 1.3 nCPM
- differentiating spermatogonia: 1.2 nCPM
- distal convoluted tubule cells: 1.2 nCPM
Immune cell
- naive B-cell: 7.3 nTPM
- memory B-cell: 6.9 nTPM
- plasmacytoid DC: 1.7 nTPM
- NK-cell: 0.2 nTPM
- total PBMC: 0.1 nTPM
- basophil: 0 nTPM
Brain region
- choroid plexus: 2.7 nTPM
- cerebral cortex: 2.3 nTPM
- midbrain: 1.3 nTPM
- pons: 1.3 nTPM
- white matter: 1.3 nTPM
- basal ganglia: 1.1 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)
- 1.47
- gnomAD pLI
- 0.47
- gnomAD missense Z
- 0.14
- DepMap mean gene effect
- 0.02
- DepMap dependency class
- none
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
- midbrain development
- multicellular organism growth
- post-embryonic development
- regulation of transcription by RNA polymerase II
- thalamus development
Molecular functions
- DNA binding
- DNA-binding transcription factor activity, RNA polymerase II-specific
- protein dimerization activity
- RNA polymerase II cis-regulatory region sequence-specific DNA binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of TAL2 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 TAL2 as an antibody target. Whether an autoantibody or antibody against TAL2 could matter depends on whether native TAL2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
TAL2 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 TAL2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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