PIP4P1
Type 1 phosphatidylinositol 4,5-bisphosphate 4-phosphatase
Also known as: C14orf9, MGC26684, PP4P1_HUMAN, TMEM55B
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q86T03
- Gene
- PIP4P1
- Ensembl
- ENSG00000165782
- Chromosome
- 14
- Canonical length
- 277 aa
- Protein class
- Enzymes, Metabolic proteins, Predicted intracellular proteins, Predicted membrane proteins
OverviewNCBI Gene
TMEM55B catalyzes the degradation of phosphatidylinositol 4,5-bisphosphate (PtdIns-4,5-P2) by removing the 4-phosphate (Ungewickell et al., 2005 [PubMed 16365287]).[supplied by OMIM, Mar 2008]
Canonical amino-acid sequenceUniProt
277 residues, UniProt reviewed canonical sequence.
>Q86T03|PIP4P1
1 MAADGERSPL LSEPIDGGAG GNGLVGPGGS GAGPGGGLTP SAPPYGAAFP PFPEGHPAVL
61 PGEDPPPYSP LTSPDSGSAP MITCRVCQSL INVEGKMHQH VVKCGVCNEA TPIKNAPPGK
121 KYVRCPCNCL LICKVTSQRI ACPRPYCKRI INLGPVHPGP LSPEPQPMGV RVICGHCKNT
181 FLWTEFTDRT LARCPHCRKV SSIGRRYPRK RCICCFLLGL LLAVTATGLA FGTWKHARRY
241 GGIYAAWAFV ILLAVLCLGR ALYWACMKVS HPVQNFSLocalizationUniProt · AlphaFold · HPA
Whether an antibody against PIP4P1 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
- Cell surface
- Secreted
- No
- Transmembrane segments
- 2
- Mean surface accessibility (rSASA)
- 0.5
- Highest tissue expression
- 46 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 46 nTPM
- cerebral cortex: 40 nTPM
- skeletal muscle: 34 nTPM
- skin: 33 nTPM
- cerebellum: 32 nTPM
- hypothalamus: 31 nTPM
Single-cell type
- syncytiotrophoblasts: 204 nCPM
- cytotrophoblasts: 93 nCPM
- oocytes: 78 nCPM
- esophageal apical cells: 74 nCPM
- hofbauer cells: 71 nCPM
- migrating cytotrophoblasts: 56 nCPM
Immune cell
- memory B-cell: 13 nTPM
- plasmacytoid DC: 10 nTPM
- naive B-cell: 10 nTPM
- eosinophil: 7.3 nTPM
- naive CD8 T-cell: 6.1 nTPM
- naive CD4 T-cell: 5.8 nTPM
Brain region
- pons: 33 nTPM
- hypothalamus: 30 nTPM
- cerebral cortex: 29 nTPM
- thalamus: 29 nTPM
- basal ganglia: 28 nTPM
- midbrain: 28 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)
- 0.4
- gnomAD pLI
- 0.87
- DepMap mean gene effect
- -0.07
- 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
- cholesterol metabolic process
- lysosome localization
- phosphatidylinositol dephosphorylation
- phospholipid metabolic process
- positive regulation of TORC1 signaling
- proton-transporting V-type ATPase complex assembly
- regulation of signal transduction by p53 class mediator
- response to sterol depletion
Molecular functions
- 5-bisphosphate 4-phosphatase activity
- phosphatidylinositol-4
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of PIP4P1 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 PIP4P1 as an antibody target. Whether an autoantibody or antibody against PIP4P1 could matter depends on whether native PIP4P1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
PIP4P1 is annotated at the cell surface, where native PIP4P1 is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label PIP4P1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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