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RASD1 (human)

Overview RASD1 Small GTPase. Negatively regulates the transcription regulation activity of the APBB1/FE65-APP complex via its interaction with APBB1/FE65. Forms a ternary complex with CAPON and NOS1. Component of a complex, at least composed of APBB1, RASD1/DEXRAS1 and APP. Interacts with APBB1/FE65. By dexamethasone. Expressed in a variety of tissues including heart, cardiovascular tissues, brain, placenta, lung, liver, skeletal muscle, kidney, pancreas, gastrointestinal and reproductive tissues. Belongs to the small GTPase superfamily. RasD family. Note: This description may include information from UniProtKB. Protein type: G protein, monomeric (RasD) Cellular Component: perinuclear region of cytoplasm; plasma membrane; nucleus Molecular Function: GTPase activity; GTP binding Biological Process: G-protein coupled receptor protein signaling pathway; small GTPase mediated signal transduction; signal transduction; negative regulation of transcription, DNA-dependent; nitric oxide mediated signal transduction Reference #:  Q9Y272 (UniProtKB) Alt. Names/Synonyms: activator of G protein signaling; Activator of G-protein signaling 1; AGS1; Dexamethasone-induced Ras-related protein 1; DEXRAS1; MGC:26290; RAS, dexamethasone-induced 1; ras-related protein; RASD1 Gene Symbols: RASD1 Molecular weight: 31,642 Da Basal Isoelectric point: 9.15  Predict pI for various phosphorylation states Protein-Specific Antibodies or siRNAs from Cell Signaling Technology®

Select Structure to View Below RASD1

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	Modification Sites and Domains

	Modification Sites in Parent Protein, Orthologs, and Isoforms

SS  SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.	MS  MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.			human
0	1		S202-p	AKLPSEMsPDLHRKV

	mouse
S202	AKLPSEMSPDLHRKV

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