Target intelligence / Profile preview

Phosphatidylinositol transfer protein alpha (PITPNA)

Target
PITPNA
Molecular classification
Lipid transfer/binding protein, Soluble transporter (cytosolic phospholipid transporter), Member of the SRPBCC (START/RHOalphaC/PITP/Bet v1/CoxG/CalC) domain superfamily[1][3]
01

Overview

Phosphatidylinositol transfer protein alpha (PITPNA) is a highly conserved soluble protein found ubiquitously in eukaryotic cells[1][2][3][4]. It catalyzes the exchange and transfer of phospholipids, notably phosphatidylinositol (PI) and phosphatidylcholine (PC), between intracellular membranes, most prominently from the endoplasmic reticulum to other cellular compartments[1][2][3][4]. PITPNA is a key player in maintaining the proper phospholipid composition of membranes and in supporting signal transduction by presenting PI directly to kinases and phospholipases[1][2][4]. It is vital for important cellular processes including vesicular trafficking, phospholipase C-mediated signaling, exocytosis, and regulated secretion[1][2][3]. Loss or mutation of PITPNA results in neurological deficits in model organisms and is associated with defects in platelet signal transduction, tumor metastasis, and possibly inherited retinal degeneration by analogy with related proteins in other species[1][4]. There are no well-established small molecule drugs targeting PITPNA, nor known approved drug interactions or established biomarker applications in clinical practice, as its principal biological roles are essential and predominantly intracellular[1][2][4].

Other names
Phosphatidylinositol transfer protein alpha isoformPITPNAPITPNPI-TP-alphaPtdIns transfer protein alphaPtdInsTP alphaVIB1AHEL-S-36PI-TPalphaphosphatidylinositol transfer protein alpha isoformEpididymis secretory protein Li 36ptdIns transfer protein alphaptdInsTP alpha
02

Biological functions

Phospholipid transfer (phosphatidylinositol and phosphatidylcholine) between intracellular membranes[1][2][4]Regulation of signal transduction, especially phosphoinositide signaling pathways[1][4]Vesicular/secretory trafficking[1][2]Regulator in exocytosis[2][3]Maintenance of membrane phospholipid composition[1][4]
03

Disease associations

Neurodegeneration (mutations/deficiency cause neurodegeneration in animal models)[1]Platelet signaling disorders[4]Cancer/tumor metastasis (impaired function affects tumor dissemination via platelet signaling)[4]Retinal degeneration (by homology to RdgB-related proteins in Drosophila)[1]
04

Safety considerations

Loss-of-function mutations can lead to neurodegeneration[1]Deficiency disrupts platelet function and can impair hemostasis and promote tumor dissemination[4]Essential for proper signal transduction, so profound loss is lethal in model systems[1][4]

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