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Rabbit Anti-GRAF/FITC Conjugated antibody
background:
Cellular signaling by G-proteins is down-regulated by GTPase-activating proteins (GAPs), which increase the rate of GTP hydroylsis. The GTPase regulator associated with focal adhesion kinase (GRAF) has GAP activity toward Rho A and Cdc42, but not Rac1. GRAF is ubiquitously expressed with high levels in heart and brain. Expression of GRAF causes clearing of stress fibers and formation of long actin based filopodial-like extensions. Fusion of MLL with GRAF, MLL/GRAF, is included in a rare genetic subgroup of acute myeloid leukemia (AML) cases.
Function:
GTPase-activating protein for RHOA and CDC42.
Subunit:
Interacts with NYAP1, NYAP2 and MYO16 (By similarity). Binds to the SLCterminus of PTK2/FAK1.
Subcellular Location:
Cell junction; focal adhesion. Cytoplasm; cytoskeleton. Colocalizes with actin stress fibers and cortical actin structures.
DISEASE:
Defects in ARHGAP26 are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. Chromosomal translocation t(5;11)(q31;q23) with MLL has been found in a JMML patient.
Similarity:
Contains 1 PH domain.
Contains 1 Rho-GAP domain.
Contains 1 SH3 domain.
Database links:
Entrez Gene: 23092 Human
Entrez Gene: 71302 Mouse
Entrez Gene: 307459 Rat
Omim: 605370 Human
SwissProt: Q9UNA1 Human
SwissProt: Q6ZQ82 Mouse
Unigene: 654668 Human
Unigene: 329396 Mouse
Unigene: 214162 Rat
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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