RAP1GAP Products

Description

Rap1GAP, an 85/95kDa protein, is a member of a family of GAP's specific for Rap1 (1). Though to be an important tumor suppressor, Rap1GAP has no sequence homology with other GAPs such as RasGAP, RanGAP and RhoGAP. Purified as a cytosolic and membrane-bound protein, both isoforms consist of two monomers each contain a dimerization and a catalytic domain (2-4). Mutations in the GAP domain of the tumor suppressor tuberin, can cause benign tumor phenotype tuberous sclerosis (5).

Bioinformatics

Entrez	5909 Human 110351 Mouse 298570 Rat
Uniprot	P47736 Human NP_002876 Human AAH54490 Human AAH54490.1 Human
Product By Gene ID	5909
Alternate Names	GTPase activating protein 1 RAP1 GTPase activating protein

Diseases related to RAP1GAP

Discover more about diseases related to RAP1GAP.

Neoplasms
Malignant Neoplasms
Tissue Adhesions
Carcinoma
Cell Invasion
Tuberous Sclerosis
Sclerosis
Melanoma
Malignant Neoplasm Of Thyroid
Neoplasm Invasiveness
Tumor Progression
Thyroid Neoplasm
Cell Transformation, Neoplastic
Malignant Squamous Cell Neoplasm
Kidney Neoplasm
Tuberous Sclerosis 2 (disorder)
Neoplasm Metastasis
Hamartoma
Carcinogenesis

Pathways for RAP1GAP

View related products by pathway and learn more about each of the pathways below.

Cell Adhesion
Cell Proliferation
Cell Migration
Cell Growth
Integrin Activation
Pathogenesis
Cell Cycle
Methylation
Cell Differentiation
Mitosis
Localization
Oncogenesis
Membrane Depolarization
Endocytosis
Rna Interference
Secretion
Fibroblast Proliferation
Tropism
Cell Division
Fibroblast Activation

Research Areas for RAP1GAP

Find related products by research area and learn more about each of the different research areas below.

Cellular Markers
Lysosome Markers

PTMs for RAP1GAP

Learn more about PTMs related to RAP1GAP.

Phosphorylation
Methylation
Demethylation
Cleavage
Ubiquitination

Bioinformatics Tool for RAP1GAP

Discover related pathways, diseases and genes to RAP1GAP. Need help? Read the Bioinformatics Tool Guide for instructions on using this tool.