Target intelligence / Profile preview

Inositol polyphosphate-5-phosphatase F (INPP5F)

Target
INPP5F
Molecular classification
Enzyme (phosphatase, specifically inositol polyphosphate 5-phosphatase), Sac domain phosphatase superfamily
01

Overview

Inositol polyphosphate-5-phosphatase F (INPP5F) is a large membrane-associated enzyme (128 kDa, 1132 amino acids) containing a Sac domain and is primarily responsible for dephosphorylating specific phosphoinositides, particularly phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate. These actions position it as a modulator of key cellular processes such as endocytic recycling, cell migration, signal transduction, and STAT3/AKT pathway regulation. INPP5F plays roles in cardiac physiology, neural regeneration, and has implications for cancer biology and other diseases. No directly interacting drugs are listed in pharmacogenomic resources. As an enzyme modifying phosphoinositide signaling, it shares molecular relationships with OCRL and other Sac domain phosphatases, distinguishing its function from related phosphatases in cellular homeostasis and disease[1][2][3][4][5].

Other names
SAC2KIAA0966hSAC2Phosphatidylinositide phosphatase SAC2Sac domain-containing inositol phosphatase 2Sac domain-containing phosphoinositide 4-phosphatase 2Sac domain-containing phosphoinositide 5-phosphatase 2MSTP007MSTP047
02

Mechanism of action

Dephosphorylation of phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate at the 5-position, impacting downstream PI3K/AKT and STAT3 pathways

03

Biological functions

Phosphoinositide metabolism (dephosphorylation of phosphatidylinositol phosphates)Regulation of receptor recycling and integrin recyclingModulation of cell migrationRegulation of AKT/GSK3B signaling pathwayNegative regulation of STAT3 signalingModulation of cardiac myocyte size and cardiac response to stressNegative regulation of axon regeneration after central nervous system injuriesEndocytic recycling
04

Disease associations

Cancer (roles through modulation of cell growth and receptor recycling pathways)Cardiovascular disease (involvement in cardiac myocyte response to stress)Neurodegenerative disease/neurological recovery (negative regulator of axon regeneration)Foramen magnum meningiomaAlbinismOculocutaneous type Ia
05

Safety considerations

Inhibition may increase risk of cardiac hypertrophy or exacerbate neurological injury due to loss of negative regulatory functions.Targeting this enzyme could affect multiple downstream signaling pathways, leading to potential off-target effects on cell migration, proliferation, and survival.

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