RASD1
RASD1 (ras related dexamethasone induced 1, also known as DEXRAS1 and AGS1) is a small GTPase of the Ras superfamily that is induced by dexamethasone. It acts as an activator of G-protein signalling and interacts with the adaptor proteins CAPON and FE65. Browse Assay Genie's current range of RASD1 research reagents below, or read on for the biology behind the target.
RASD1 is a small GTPase that belongs to the RasD family within the wider small GTPase superfamily. It is described as an activator of G-protein signalling and acts as a direct nucleotide exchange factor for Gi-Go proteins. It also negatively regulates the transcription regulation activity of the APBB1/FE65-APP complex through its interaction with APBB1/FE65.
The RASD1 protein is annotated at the cell membrane, in the perinuclear region of the cytoplasm and in the nucleus. It interacts with the neuronal nitric oxide adaptor protein CAPON and with the nuclear adaptor protein FE65, which in turn interacts with the Alzheimer's disease amyloid precursor protein. The RASD1 gene has orthologues in mouse and rat, both named Rasd1, and alternatively spliced transcript variants encoding different isoforms have been reported.
The name reflects its induction by dexamethasone. The RASD1 gene may play a role in dexamethasone-induced alterations in cell morphology, growth and cell-extracellular matrix interactions. Epigenetic inactivation of the gene is closely correlated with resistance to dexamethasone in multiple myeloma cells. Earlier designations include RAS, dexamethasone-induced 1, as well as the symbols DEXRAS1 and AGS1, which still appear in the literature.
RASD1 acts as a direct nucleotide exchange factor for Gi-Go proteins, making it a useful subject for studies of G-protein activation.
Expression of RASD1 is induced by dexamethasone, and it may contribute to dexamethasone-driven changes in cell morphology, growth and matrix interactions.
Epigenetic inactivation of RASD1 is closely correlated with dexamethasone resistance in multiple myeloma cells.
RASD1 binds CAPON and FE65, linking it to nitric oxide adaptor biology and to the APBB1/FE65-APP complex relevant to Alzheimer's disease.
RASD1 is a small GTPase that activates G-protein signalling, acting as a direct nucleotide exchange factor for Gi-Go proteins. It also negatively regulates the transcription regulation activity of the APBB1/FE65-APP complex by interacting with APBB1/FE65.
RASD1 is also known as DEXRAS1 and AGS1, and was previously named RAS, dexamethasone-induced 1. The UniProt protein name is Dexamethasone-induced Ras-related protein 1. Alternatively spliced transcript variants encoding different isoforms have been found for the gene.
Epigenetic inactivation of RASD1 is closely correlated with dexamethasone resistance in multiple myeloma cells. Its protein partner FE65 interacts with the Alzheimer's disease amyloid precursor protein. Mouse and rat both carry a Rasd1 orthologue; check the datasheet of any product for its validated reactivity.
Related small GTPases, adaptor proteins and pathway partners of RASD1 with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9Y272; product specifications from Assay Genie datasheets.