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FLASH GENE

Symbol

ABL2

contributors: mct - updated : 22/11/2008

HGNC name	v-abl Abelson murine leukemia viral oncogene homolog 2 (arg, Abelson-related gene)
HGNC id	77

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type

widely

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Digestive liver       highly   salivary gland       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Connective bone       Muscular striatum skeletal   highly

cell lineage
cell lines	tumors cell lines
fluid/secretion

at STAGE

physiological period

fetal

Text	developing neurons

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	two Src homology domain SH3, SH2 and a tyrosine kinase catalytic domain
	two filamentous F and G actin-binding domain at the C terminus

HOMOLOGY

interspecies

homolog to Abelson murine leukemia viral (v-abl) oncogene 2

intraspecies

homolog to ABL1

Homologene

FAMILY	TYR family of protein kinase
	ABL subfamily

CATEGORY

enzyme , protooncogene

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm,cytoskeleton

basic FUNCTION	non receptor, tyrosine kinase regulating actin cytoskeletal structure
	membrane-anchored nonreceptor tyrosine kinase that is a novel mediator of SEMA3F-induced RhoA inactivation and collapsing activity
	has a role in cytoskeletal rearrangements by its C-terminal F-actin- and microtubule-binding sequences

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

signal transduction

a component

INTERACTION

DNA

RNA

small molecule

protein	ARGBP2, potentially linking Abl family kinases and the actin cytoskeleton
	interacting with SEMA3F (in response to SEMA3F, is recruited to bind plexin A1 and to phosphorylate and activate p190RhoGAP directly, resulting in RhoA inactivation and cofilin-mediated cytoskeleton collapse)
	interacting with SIVA1 (functional significance of the ABL2-SIVA1 interaction is supported by the finding that ABL2 is activated by oxidative stress and that this response involves ABL2-mediated phosphorylation of SIVA1 on Tyr(48) (Cao 2001)

cell & other

REGULATION

activated by

oxidative stress induces apoptosis by a SIVA1-dependent mechanism (Cao 2001)

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral fusion       with ETV6 in t(1;12)(q25;p13) in acute myeloid leukmia

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS