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Inositol Polyphosphate Phosphatases in Human Disease

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Phosphoinositides and Disease

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 362))

Abstract

Phosphoinositide signalling molecules interact with a plethora of effector proteins to regulate cell proliferation and survival, vesicular trafficking, metabolism, actin dynamics and many other cellular functions. The generation of specific phosphoinositide species is achieved by the activity of phosphoinositide kinases and phosphatases, which phosphorylate and dephosphorylate, respectively, the inositol headgroup of phosphoinositide molecules. The phosphoinositide phosphatases can be classified as 3-, 4- and 5-phosphatases based on their specificity for dephosphorylating phosphates from specific positions on the inositol head group. The SAC phosphatases show less specificity for the position of the phosphate on the inositol ring. The phosphoinositide phosphatases regulate PI3K/Akt signalling, insulin signalling, endocytosis, vesicle trafficking, cell migration, proliferation and apoptosis. Mouse knockout models of several of the phosphoinositide phosphatases have revealed significant physiological roles for these enzymes, including the regulation of embryonic development, fertility, neurological function, the immune system and insulin sensitivity. Importantly, several phosphoinositide phosphatases have been directly associated with a range of human diseases. Genetic mutations in the 5-phosphatase INPP5E are causative of the ciliopathy syndromes Joubert and MORM, and mutations in the 5-phosphatase OCRL result in Lowe’s syndrome and Dent 2 disease. Additionally, polymorphisms in the 5-phosphatase SHIP2 confer diabetes susceptibility in specific populations, whereas reduced protein expression of SHIP1 is reported in several human leukaemias. The 4-phosphatase, INPP4B, has recently been identified as a tumour suppressor in human breast and prostate cancer. Mutations in one SAC phosphatase, SAC3/FIG4, results in the degenerative neuropathy, Charcot-Marie-Tooth disease. Indeed, an understanding of the precise functions of phosphoinositide phosphatases is not only important in the context of normal human physiology, but to reveal the mechanisms by which these enzyme families are implicated in an increasing repertoire of human diseases.

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Abbreviations

ADAM:

A disintegrin and a metalloprotease

ALL:

Acute lymphoblastic leukaemia

AML:

Acute myeloid leukaemia

AP:

Adaptor protein

APPL1:

Adaptor protein containing Pleckstrin homology domain, PTB domain and Leucine Zipper motif 1

AR:

Androgen receptor

ARF-GAP:

ADP-ribosylation factor GTPase activating protein

ARF-GEF:

ADP-ribosylation factor Guanine nucleotide-exchange factor

ASH:

Abnormal spindle-like microcephaly-associated protein/spindle pole body/hydrin

ASPM:

Abnormal spindle-like microcephaly-associated protein

ATLL:

Adult T cell leukaemia/lymphoma

AVP:

Arginine vasopressin

BAFF:

B cell activating factor belonging to the TNF family

BCR:

B cell receptor

BMM:

Bone marrow macrophage

BMMC:

Bone marrow mast cell

Btk:

Bruton’s tyrosine kinase

C. elegans :

Caenorhabditis elegans

C/EBPβ:

CCAAT enhancer-binding protein β

CAP:

Cbl interacting protein

CD2AP:

CD2-associated protein

Cdk5:

Cyclin-dependent kinase 5

CD-MPR:

Cation-dependent mannose-6-phosphate receptor

CI-MPR:

Cation-independent mannose-6-phosphate receptor

CK5/6:

Cytokeratin 5/6

CLL:

Chronic lymphocytic leukaemia

CML:

Chronic myeloid leukaemia

CMT:

Charcot-Marie-Tooth

CRMP2:

Collapsin response mediator protein 2

DAP12:

DNAX-activating protein of 12 kD

DC:

Dendritic cell

DS:

Down’s syndrome

EGFR:

Epidermal growth factor receptor

Epo:

Erythropoietin

ER:

Endoplasmic reticulum

ER:

Oestrogen receptor

ER− :

Oestrogen receptor negative

ER+ :

Oestrogen receptor positive

ERGIC:

Endoplasmic reticulum-to-Golgi intermediate compartment

F. tularensis :

Francisella tularensis

F-MuLV:

Friend murine leukaemia virus

FYVE:

Fab1, YOTB, Vac1, EEA1

G6Pase:

Glucose-6-phosphatase

GAP:

GTPase activating protein

G-CSF:

Granulocyte colony-stimulating factor

GIPC:

GAIP-interacting protein C terminus

GK:

Goto Kakizaki

GSK3β:

Glycogen synthase kinase-3 β

HDAC2:

Histone deacetylase 2

HER-2:

v-erb-b2 erythroblastic leukaemia viral oncogene homologue 2

IGF-1:

Insulin-like growth factor

INPP4A:

Inositol polyphosphate 4-phosphatase type I

INPP4B:

Inositol polyphosphate 4-phosphatase type II

INPP5A:

Inositol polyphosphate 5-phosphatase type I

INPP5B:

Inositol polyphosphate 5-phosphatase type II

INPP5E:

Inositol polyphosphate 5-phosphatase type IV

Ins(1,2,3,4,5)P5 :

Inositol 1,2,3,4,5-pentakisphosphate

Ins(1,3,4)P3 :

Inositol 1,3,4-trisphosphate

Ins(1,3,4,5)P4 :

Inositol 1,3,4,5-tetrakisphosphate

Ins(1,4)P2 :

Inositol 1,4-bisphosphate

Ins(1,4,5)P3 :

Inositol 1,4,5-trisphosphate

Ins(1,4,5,6)P4 :

Inositol 1,4,5,6-tetrakisphosphate

Ins(3,4)P2 :

Inositol 3,4-bisphosphate

IRS:

Insulin receptor substrate

ITIM:

Immunoreceptor tyrosine-based inhibitory motif

LAT:

Linker for activation of T cells

M-CSF:

Monocyte colony-stimulating factor

MDS:

Miller–Dieker syndrome

MEFs:

Mouse embryonic fibroblasts

miR-155:

MicroRNA-155

MNB/DYRK1A:

Dual-specific tyrosine phosphorylation-regulated kinase 1A

NCA:

Na+/Ca2+ antiporter

NCoR:

Nuclear corepressor

NF-κB:

Nuclear factor-κB

NPF:

Asparagine-proline-phenylalanine

NTAL:

Non-T cell activation linker

OCRL:

Oculocerebrorenal syndrome of Lowe

PAS:

(PIKfyve–ArPIKfyve–Sac3)

PBMs:

Peripheral blood monocytes

PDGF:

Platelet-derived growth factor

PDK1:

Phosphoinositide-dependent kinase-1

PEPCK:

Phosphoenolpyruvate carboxykinase

PGN:

Peptidoglycan

PH:

Pleckstrin homology

PI:

Phosphoinositide

PI(3)P:

Phosphatidylinositol 3-phosphate

PI(3,4)P2 :

Phosphatidylinositol 3,4-bisphosphate

PI(3,4,5)P3 :

Phosphatidylinositol 3,4,5-trisphosphate

PI(3,5)P2 :

Phosphatidylinositol 3,5-bisphosphate

PI(4)P:

Phosphatidylinositol 4-phosphate

PI(4,5)P2 :

Phosphatidylinositol 4,5-bisphosphate

PI(5)P:

Phosphatidylinositol 5-phosphate

PI3K:

Phosphatidylinositol 3-kinase

PIPP:

Proline-rich inositol polyphosphate 5-phosphatase

PLCγ:

Phospholipase C γ

PLD:

Phospholipase D

PR:

Progesterone receptor

PTB:

Phosphotyrosine binding

PTEN:

Phosphatase and tensin homolog

RANKL:

Receptor activator of nuclear factor-κB ligand

Rho-GEFs:

Rho-Guanine nucleotide exchange factors

S. flexneri :

Shigella flexneri

SAC:

Supressor of actin

SCC:

Squamous cell carcinoma

SCF:

Stem cell factor

SCIPs:

SAC domain-containing inositol phosphatases

SCVs:

Salmonella containing vacuoles

SF:

Steel-factor

SHIP:

SH2-containing inositol phosphatase

SKIP:

Skeletal muscle and kidney inositol phosphatase

SNP:

Single nucleotide polymorphism

SODD/BAG4:

Silencer of death domain

SPD2:

Spindle pole body 2

SYNJ1:

Synaptojanin 1

SYNJ2:

Synaptojanin 2

T-ALL:

T cell acute lymphoblastic leukaemia

TGFβ:

Transforming growth factor β

TGN:

Trans-Golgi network

Tir:

Translocated intimin receptor

TIRFM:

Total internal reflection fluorescent microscopy

TLR-2:

Toll-like receptor-2

TMEM55A:

Transmembrane protein 55A

TMEM55B:

Transmembrane protein 55A

TREM2:

Triggering receptor expressed on myeloid cells-2

UTR:

Untranslated region

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  1. Department of Biochemistry and Molecular Biology, Monash University, Wellington Rd, Clayton, 3800, Australia

    Sandra Hakim, Micka C. Bertucci, Sarah E. Conduit, David L. Vuong & Christina A. Mitchell

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  1. Sandra Hakim
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  2. Micka C. Bertucci
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  4. David L. Vuong
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Correspondence to Christina A. Mitchell .

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  1. CTR DIABETES BARTS, Queen Mary University of London, UK, NEWARK ST 4, LONDON E1 2AT, United Kingdom

    MARCO FALASCA

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Hakim, S., Bertucci, M.C., Conduit, S.E., Vuong, D.L., Mitchell, C.A. (2012). Inositol Polyphosphate Phosphatases in Human Disease. In: FALASCA, M. (eds) Phosphoinositides and Disease. Current Topics in Microbiology and Immunology, vol 362. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-5025-8_12

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