Koska inositoliaineenvaihdunta kiertää vesiliukoisesta ja rasvaliukoiseen aitioon ja takaisin on fosfataaseissa niitä, jotka vaikuttavat a) lipidiliukoisiin fosfoinositideihin (PI, lipositolit) ja b) vesiliukoisiin jonistolifosfaattilajeihin (IPx)
Sisällysluettelossa on seuraavia
vesiliukoisia fosfataaseja mainittu:
INPP4A, Inositolipolyfosfaatti 4-fosfataasi tyyppi 1
INPP4B, Inositolipolyfosfaatti 4-fosfataasi tyyppi 2
INPP5J, Inositolipolyfosfaatti 5-fosfataasi J
INPP5K, Inositolipolyfosfatti 5-fosfataasi K
PIPP, proliinipitoinen inositolipolyfosfaattifosfataasi
SHIP1, SH2 domeenin sisältävä inositolifosfaasi 1
SHIP2, SH2 domeenin sisältävä isositolifosfataasi 2
SKIP, lihakseen ja munuaiseen rikastunut inositol polyfosfaattifosfataasi
Rasvaliukoiseen fosfoinositidiin vaikuttaa
PTEN , fosfataasi ja tensiinihomologi
PTPN9, PTP-MEG2 (T-soluissa polyfosfoinositideihin esim.)
Myotubulariini MTMR2 on fosfoinositidifosfataasi .
https://www.sciencedirect.com/science/article/pii/S1044579X18301159?via%3Dihub
Review
Phosphoinositide phosphatases in cancer cell dynamics—Beyond PI3K and PTEN
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Phosphoinositides (PIs) are a group of lipids that regulate
intracellular signaling and subcellular biological events. The signaling by PIP3,
phosphatidylinositol-3,4,5-trisphosphate and Akt mediates the action of
growth factors that are essential for
cell proliferation,
gene transcription,
cell migration, and polarity.
The
hyperactivation of this signaling has been identified in different
cancer cells; and, it has been implicated
in oncogenic transformation
and cancer cell malignancy. Recent studies have argued the role of
phosphoinositides (PIs) in cancer cell dynamics, including
actin
cytoskeletal rearrangement at the plasma membrane and the organization
of intracellular compartments. The focus of this review is
to summarize
the impact of the activities of phosphoinositide (PI) phosphatases
on intracellular signaling r
elated to cancer cell dynamics and to
discuss how the abnormalities in the activities of the enzymes alter the
levels of phosphoinositides (PIs, lipositols) in cancer cells.
Abbreviations
ER. endoplasmic reticulum
ERM. ezrin, radixin, and Moesin
ESCC. esophageal squamous cell carcinoma
FA. focal adhesion
FAK. focal adhesion kinase
FEME. fast endophilin-mediated endocytosis
GOLPH3. Golgi phosphoprotein 3
INPP4A. inositol polyphosphate 4-phosphatase type I
INPP4B. inositol polyphosphate 4-phosphatase type II
Lpd. lamellipodin
INPP5J. inositol polyphosphate 5-phosphatase J
INPP5K. inositol polyphosphate 5-phosphatase K
LOH. loss of heterogeneity
N-WASP. neural Wiskott–Aldrich syndrome protein
PDK1. phosphoinositide-dependent kinase 1
PH. plextrin homology
PI. phosphatidylinositol
PI(3)P. phosphatidylinositol-3-monophosphate
PI(4)P. phosphatidylinositol-4-monophosphate
PI(5)P. phosphatidylinositol-5-monophosphate
PI(3,4)P2. phosphatidylinositol-3,4-bisphosphate
PI(3,5)P2. phosphatidylinositol-3,5-bisphosphate
PI(4,5)P2. phosphatidylinositol-4,5-bisphosphate
PIP3. phosphatidylinositol-3,4,5-trisphosphate
PI3K. PI 3-kinase
PI4K. phosphatidylinositol 4-kinase
PIP5K. phosphatidylinositol 4-phosphate 5-kinase
PIPP. proline-rich inositol polyphosphate 5-phosphatase
PM. plasma membrane
P-Rex. phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger
PTEN. phosphatase and tensin homolog
PX. phox homology
SAC. suppressor of actin
SHIP1, SH2 domain-containing inositol phosphatase 1
SHIP2, SH2 domain-containing inositol phosphatase 2
SKIP, skeletal muscle and kidney enriched inositol polyphosphate phosphatase
SYNJ2, synaptojanin 2
Tks5, tyrosine kinase substrate 5
Keywords
Cell migration
Cell polarity
Focal adhesion
Invadopodia
PI(3,4)P2
PIP3
Phosphoinositide phosphatase
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