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FLASH GENE

Symbol

ARHGAP26

contributors: mct - updated : 23-05-2015

HGNC name	Rho GTPase activating protein 26
HGNC id	17073

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	a N terminal nuclear localization signal (NLS)
	a PH domain
	a GTPase activating protein (GAP) domain
	an amphipathic lipid bending/sculpting BAR domain
	a SH3 C-terminal domain

HOMOLOGY

interspecies	homolog to rattus Arhgap26 (97.8 pc)
	homolog to murine Arhgap26 (96.9 pc)

Homologene

FAMILY

Rho family of GTPase-activating protein (GAP) family

CATEGORY

enzyme , regulatory

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm,cytosolic
	intracellular,cytoplasm,cytoskeleton

basic FUNCTION	acting as a negative regulator of Rho A
	GAP activity
	integrin signal transduction pathway
	might be involved in the pathogenesis of the mental retardation
	necessary and sufficient for mediating RHOA down-regulation and inducing muscle differentiation
	might serve as a key regulator of RHOA activity during myogenesis
	remodels potentially membrane microdomains at adhesion sites into endocytic carriers, facilitating membrane turnover during cell morphological changes
	is a regulator of clathrin-independent endocytosis
	its activity regulates polarity establishment

CELLULAR PROCESS

cell organization/biogenesis

PHYSIOLOGICAL PROCESS

development

text	nervous system development
	actin cytoskeleton organization and biogenesis

PATHWAY

metabolism

signaling

signal transduction

critical component of the integrin signaling transduction pathway

a component

INTERACTION

DNA

RNA

small molecule

protein	binding to the C-terminal of pp125(FAK)
	promotes skeletal muscle differentiation by limiting RHOA/ROCK1 signaling
	interacted with a network of endocytic and adhesion proteins and enriched at podosome-like adhesions and src-induced podosomes
	ARHGAP26 -mediated removal of RAB8A from the cell surface restricts its activity during protrusion formation, thereby facilitating dynamic adjustment of the polarity axis

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral fusion translocation     fusion with MLL in t(5;11)(q31;q23) in myelodysplastic syndrome tumoral   deletion     deletion in myelodysplastic syndrome tumoral       gain of function activated in malignant melanoma tumoral     --low   in myeloid malignancies constitutional     --low   decreased in ATRX patients

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

GrafF1-depleted embryos exhibited elevated RhoA activity and defective myofibrillogenesis that resulted in progressive muscle degeneration, defective motility, and embryonic lethality