Rrad Ras-related associated with diabetes [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Rradprovided by MGI
Official Full Name: Ras-related associated with diabetesprovided by MGI
Primary source: MGI:MGI:1930943
See related: Ensembl:ENSMUSG00000031880 AllianceGenome:MGI:1930943
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Rad; REM3
Summary: Predicted to enable GTP binding activity and calcium channel regulator activity. Predicted to be involved in negative regulation of cell growth. Located in plasma membrane. Is expressed in several structures, including alimentary system; central nervous system; genitourinary system; hemolymphoid system gland; and musculature. Human ortholog(s) of this gene implicated in type 2 diabetes mellitus. Orthologous to human RRAD (RRAD, Ras related glycolysis inhibitor and calcium channel regulator). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Biased expression in heart adult (RPKM 81.0), ovary adult (RPKM 10.3) and 10 other tissues See more
Orthologs: human all
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Genomic context

Location:: 8 D3; 8 53.04 cM

Exon count:: 5

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	8	NC_000074.7 (105354702..105357921, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	8	NC_000074.6 (104628070..104631350, complement)

Chromosome 8 - NC_000074.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.
Title: L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.
Compared to normal adipocytes, slincRAD knockdown cells had defective differentiation features, such as smaller sizes and decreased lipid production. For elder mice, slincRAD knockdown led to abnormal glucose and lipid metabolism.
Title: Knockdown of slincRAD leads to defective adipose development in vivo.
we report that Rad GTPase function is required for normal bone homeostasis in mice
Title: Rad GTPase is essential for the regulation of bone density and bone marrow adipose tissue in mice.
Rad reduction provides a stable inotropic response rooted in sarcomere level function in hearts of knockout mice.
Title: Rad-deletion Phenocopies Tonic Sympathetic Stimulation of the Heart.
The Rad(-/-) phenotype is marked by enhanced systolic and diastolic function, which is consistent with a model that does not progress into heart failure.
Title: Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging.
Rad, Gem and Rem all reduce depolarization-dependent Ca2+ entry in developing myotubes.
Title: RGK protein-mediated impairment of slow depolarization- dependent Ca2+ entry into developing myotubes.
A dominant-negative Rad mutation causes arrhythmogenesis via PKA-mediated phosphorylation of RYR2 activity in the heart.
Title: Suppression of Rad leads to arrhythmogenesis via PKA-mediated phosphorylation of ryanodine receptor activity in the heart.
Depletion of Rad GTPase increases L-type calcium channel current leading to increased cardiac contraction, without stimulating cardiac hypertrophy.
Title: Rad GTPase deletion increases L-type calcium channel current leading to increased cardiac contraction.
Mouse Rad Q65P (the murine equivalent of human Rad Q66P) inhibits L-type currents conducted by CaV1.2 or CaV1.3 channels as potently as wild-type Rad (>95% inhibition of both channels).
Title: Potent inhibition of L-type Ca2+ currents by a Rad variant associated with congestive heart failure.
Rad GTPase inhibits cardiac fibrosis through connective tissue growth factor in failing hearts.
Title: Rad GTPase inhibits cardiac fibrosis through connective tissue growth factor.

Submit: New GeneRIF Correction See all GeneRIFs (14)

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Targeted (3) 1 citation
Endonuclease-mediated (1)

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables GTP binding	IBA Inferred from Biological aspect of Ancestor more info
enables GTPase activity	IEA Inferred from Electronic Annotation more info
enables calcium channel regulator activity	IBA Inferred from Biological aspect of Ancestor more info
enables calmodulin binding	IEA Inferred from Electronic Annotation more info
enables nucleotide binding	IEA Inferred from Electronic Annotation more info
enables protein binding	IPI Inferred from Physical Interaction more info	PubMed

Process	Evidence Code	Pubs
involved_in negative regulation of cell growth	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of high voltage-gated calcium channel activity	IEA Inferred from Electronic Annotation more info

Component	Evidence Code	Pubs
located_in T-tubule	IDA Inferred from Direct Assay more info	PubMed
located_in membrane	IEA Inferred from Electronic Annotation more info
is_active_in plasma membrane	IBA Inferred from Biological aspect of Ancestor more info
located_in plasma membrane	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: GTP-binding protein RAD

Names: Ras-like GTP-binding protein rad

NP_001412596.1

EC 3.6.5.2

NP_062636.2

EC 3.6.5.2

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.