Target intelligence / Profile preview

Proline-rich acidic protein 1 (PRAP1)

Target
PRAP1
Molecular classification
Other (secreted, intrinsically disordered protein), Lipid-binding protein
01

Overview

Proline-rich acidic protein 1 (PRAP1) is a 17 kDa, 149-amino acid secreted, intrinsically disordered protein highly expressed in the gastrointestinal epithelium and present in other tissues such as epididymis and uterus. PRAP1 facilitates lipid absorption by directly binding triglycerides and phospholipids, acting in concert with MTTP to promote formation and secretion of apoB-containing lipoproteins (including chylomicrons and VLDL). PRAP1 is also implicated in protecting epithelial cells from apoptosis following irradiation, by limiting DNA damage responses and p21 expression in a p53-dependent manner. It interacts with the mitotic checkpoint protein MAD1, modulating cell cycle progression and has noted down-regulation in certain cancers such as hepatocellular carcinoma. PRAP1 orthologs are conserved in placental mammals and its absence or mutation in mice causes abnormal lipid absorption and increased intestinal length. PRAP1 is not an established pharmacological target and no drugs or clinical biomarkers directly involve PRAP1 at present.

Other names
PRAP1PRO1195UPAUNQ608/PRO1195Epididymis tissue protein Li 178Uterine-specific proline-rich acidic proteinEpididymis secretory sperm binding proteinPRAP1_HUMAN
02

Biological functions

Lipid absorption via facilitating MTTP (microsomal triglyceride transfer protein)-mediated lipid transferPromotion of chylomicron and VLDL particle assemblyProtection of gastrointestinal epithelium from irradiation-induced apoptosis (cell death)DNA damage response (modulation of p53-dependent signaling)Negative regulation of apoptosis in epithelial cellsSuppression of mitotic spindle assembly checkpoint via MAD1 interaction
03

Disease associations

Cancer, notably hepatocellular carcinoma (modulation of mitotic checkpoint and cell cycle)Lipid metabolism disorders (potential role in hepatic steatosis and fat absorption)Gastrointestinal injury and barrier dysfunction (protection from apoptosis and irradiation)

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