HES1
Transcription factor HES-1
Also known as: bHLHb39, FLJ20408, HES-1, HES1_HUMAN, HRY
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q14469
- Gene
- HES1
- Ensembl
- ENSG00000114315
- Chromosome
- 3
- Canonical length
- 280 aa
- Protein class
- Plasma proteins, Predicted intracellular proteins, Transcription factors
- Subcellular location
- Nucleoplasm
OverviewNCBI Gene
This protein belongs to the basic helix-loop-helix family of transcription factors. It is a transcriptional repressor of genes that require a bHLH protein for their transcription. The protein has a particular type of basic domain that contains a helix interrupting protein that binds to the N-box rather than the canonical E-box. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
280 residues, UniProt reviewed canonical sequence.
>Q14469|HES1
1 MPADIMEKNS SSPVAATPAS VNTTPDKPKT ASEHRKSSKP IMEKRRRARI NESLSQLKTL
61 ILDALKKDSS RHSKLEKADI LEMTVKHLRN LQRAQMTAAL STDPSVLGKY RAGFSECMNE
121 VTRFLSTCEG VNTEVRTRLL GHLANCMTQI NAMTYPGQPH PALQAPPPPP PGPGGPQHAP
181 FAPPPPLVPI PGGAAPPPGG APCKLGSQAG EAAKVFGGFQ VVPAPDGQFA FLIPNGAFAH
241 SGPVIPVYTS NSGTSVGPNA VSPSSGPSLT ADSMWRPWRNLocalizationUniProt · AlphaFold · HPA
Whether an antibody against HES1 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
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.57
- Highest tissue expression
- 176 nTPM
Expression across tissuesHPA
Tissue
- skin: 176 nTPM
- vagina: 130 nTPM
- esophagus: 122 nTPM
- cervix: 116 nTPM
- kidney: 99 nTPM
- thyroid gland: 89 nTPM
Single-cell type
- granulosa cells: 1,612 nCPM
- enteric stem cells: 1,531 nCPM
- prostatic hillock cells: 1,246 nCPM
- epididymal basal cells: 1,238 nCPM
- prostatic club cells: 1,127 nCPM
- esophageal apical cells: 1,122 nCPM
Immune cell
- eosinophil: 16 nTPM
- non-classical monocyte: 2 nTPM
- intermediate monocyte: 1.9 nTPM
- T-reg: 0.1 nTPM
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
Brain region
- midbrain: 26 nTPM
- hypothalamus: 25 nTPM
- medulla oblongata: 22 nTPM
- basal ganglia: 20 nTPM
- thalamus: 20 nTPM
- hippocampal formation: 20 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)
- 0.57
- gnomAD pLI
- 0.71
- gnomAD missense Z
- 0.8
- DepMap mean gene effect
- 0.11
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- adenohypophysis development
- amacrine cell differentiation
- anterior/posterior pattern specification
- artery morphogenesis
- ascending aorta morphogenesis
- BMP signaling pathway
- Cajal-Retzius cell differentiation
- cardiac neural crest cell development involved in outflow tract morphogenesis
- cell adhesion
- cell fate determination
- cell maturation
- cell migration
- cell morphogenesis involved in neuron differentiation
- cellular response to fatty acid
- cellular response to interleukin-1
- cellular response to nerve growth factor stimulus
- cellular response to tumor necrosis factor
- cochlea development
- comma-shaped body morphogenesis
- common bile duct development
- embryonic heart tube morphogenesis
- establishment of epithelial cell polarity
- forebrain radial glial cell differentiation
- glomerulus vasculature development
- hindbrain morphogenesis
- inner ear auditory receptor cell differentiation
- inner ear receptor cell stereocilium organization
- labyrinthine layer blood vessel development
- lateral inhibition
- liver development
- lung development
- metanephric nephron tubule morphogenesis
- midbrain development
- midbrain-hindbrain boundary morphogenesis
- negative regulation of amacrine cell differentiation
- negative regulation of calcium ion import
- negative regulation of DNA-templated transcription
- negative regulation of forebrain neuron differentiation
- negative regulation of gene expression
- negative regulation of glial cell proliferation
- negative regulation of inner ear auditory receptor cell differentiation
- negative regulation of neuron differentiation
- negative regulation of neuron projection development
- negative regulation of oligodendrocyte differentiation
- negative regulation of pro-B cell differentiation
- negative regulation of stem cell differentiation
- negative regulation of stomach neuroendocrine cell differentiation
- negative regulation of transcription by RNA polymerase II
- nervous system development
- neuronal stem cell population maintenance
- Notch signaling pathway
- oculomotor nerve development
- outflow tract morphogenesis
- pancreatic A cell differentiation
- pharyngeal arch artery morphogenesis
- positive regulation of astrocyte differentiation
- positive regulation of BMP signaling pathway
- positive regulation of cell population proliferation
- positive regulation of DNA binding
- positive regulation of gene expression
- positive regulation of Notch signaling pathway
- positive regulation of receptor signaling pathway via JAK-STAT
- positive regulation of T cell proliferation
- positive regulation of transcription by RNA polymerase II
- positive regulation of tyrosine phosphorylation of STAT protein
- protein-containing complex assembly
- regulation of epithelial cell proliferation
- regulation of fat cell differentiation
- regulation of neurogenesis
- regulation of protein-containing complex assembly
- regulation of receptor signaling pathway via JAK-STAT
- regulation of secondary heart field cardioblast proliferation
- regulation of timing of neuron differentiation
- regulation of transcription by RNA polymerase II
- response to alkaloid
- response to Aroclor 1254
- response to thyroid hormone
- response to virus
- S-shaped body morphogenesis
- smoothened signaling pathway
- somatic stem cell population maintenance
- stomach neuroendocrine cell differentiation
- T cell proliferation
- telencephalon development
- thymus development
- ureteric bud morphogenesis
- vascular associated smooth muscle cell development
- ventricular septum development
- ventricular septum morphogenesis
- negative regulation of cell fate determination
- negative regulation of pancreatic A cell differentiation
- positive regulation of mitotic cell cycle, embryonic
- renal interstitial fibroblast development
- trochlear nerve development
Molecular functions
- chromatin binding
- DNA binding
- DNA-binding transcription factor activity, RNA polymerase II-specific
- DNA-binding transcription repressor activity, RNA polymerase II-specific
- E-box binding
- histone deacetylase binding
- HLH domain binding
- JUN kinase binding
- protein homodimerization activity
- protein-containing complex binding
- protein-folding chaperone binding
- RNA polymerase II-specific DNA-binding transcription factor binding
- sequence-specific DNA binding
- sequence-specific double-stranded DNA binding
- transcription corepressor binding
- N-box binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of HES1 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 HES1 as an antibody target. Whether an autoantibody or antibody against HES1 could matter depends on whether native HES1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
HES1 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 HES1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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