Ddit4 DNA-damage-inducible transcript 4 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Ddit4provided by MGI
Official Full Name: DNA-damage-inducible transcript 4provided by MGI
Primary source: MGI:MGI:1921997
See related: Ensembl:ENSMUSG00000020108 AllianceGenome:MGI:1921997
Gene type: protein coding
RefSeq status: PROVISIONAL
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: dig2; REDD1; Rtp801; 5830413E08Rik
Summary: Enables 14-3-3 protein binding activity. Involved in intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator. Acts upstream of or within several processes, including cellular response to dexamethasone stimulus; negative regulation of TOR signaling; and negative regulation of glycolytic process. Located in mitochondrion. Is expressed in reproductive system and retina nuclear layer. Orthologous to human DDIT4 (DNA damage inducible transcript 4). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Ubiquitous expression in spleen adult (RPKM 71.7), adrenal adult (RPKM 65.1) and 26 other tissues See more
Orthologs: human all
NEW: Try the new Gene table
Try the new Transcript table

Genomic context

Location:: 10 B4; 10 29.66 cM

Exon count:: 3

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	10	NC_000076.7 (59785497..59787592, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	10	NC_000076.6 (59949675..59951770, complement)

Chromosome 10 - NC_000076.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

Go to the top of the page Help

Go to reference sequence details

Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Expression

Go to the top of the page Help

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

Go to the top of the page Help

GeneRIFs: Gene References Into Functions

What's a GeneRIF?

NLRP3 Inflammasome Priming in the Retina of Diabetic Mice Requires REDD1-Dependent Activation of GSK3beta.
Title: NLRP3 Inflammasome Priming in the Retina of Diabetic Mice Requires REDD1-Dependent Activation of GSK3β.
Decreasing REDD1 expression protects against high glucose-induced apoptosis, oxidative stress and inflammatory injury in podocytes through regulation of the AKT/GSK-3beta/Nrf2 pathway.
Title: Decreasing REDD1 expression protects against high glucose-induced apoptosis, oxidative stress and inflammatory injury in podocytes through regulation of the AKT/GSK-3β/Nrf2 pathway.
DDIT4 Facilitates Lymph Node Metastasis via the Activation of NF-kappaB Pathway and Epithelial-Mesenchymal Transition.
Title: DDIT4 Facilitates Lymph Node Metastasis via the Activation of NF-κB Pathway and Epithelial-Mesenchymal Transition.
REDD1-dependent GSK3beta dephosphorylation promotes NF-kappaB activation and macrophage infiltration in the retina of diabetic mice.
Title: REDD1-dependent GSK3β dephosphorylation promotes NF-κB activation and macrophage infiltration in the retina of diabetic mice.
GATA2 promotes oxidative stress to aggravate renal ischemia-reperfusion injury by up-regulating Redd1.
Title: GATA2 promotes oxidative stress to aggravate renal ischemia-reperfusion injury by up-regulating Redd1.
PERK/ATF4-dependent expression of the stress response protein REDD1 promotes proinflammatory cytokine expression in the heart of obese mice.
Title: PERK/ATF4-dependent expression of the stress response protein REDD1 promotes proinflammatory cytokine expression in the heart of obese mice.
Downregulation of DDIT4 ameliorates abnormal behaviors in autism by inhibiting ferroptosis via the PI3K/Akt pathway.
Title: Downregulation of DDIT4 ameliorates abnormal behaviors in autism by inhibiting ferroptosis via the PI3K/Akt pathway.
Stress response protein REDD1 promotes diabetes-induced retinal inflammation by sustaining canonical NF-kappaB signaling.
Title: Stress response protein REDD1 promotes diabetes-induced retinal inflammation by sustaining canonical NF-κB signaling.
REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-kappaB activation.
Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation.
REDD1 Ablation Attenuates the Development of Renal Complications in Diabetic Mice.
Title: REDD1 Ablation Attenuates the Development of Renal Complications in Diabetic Mice.

Submit: New GeneRIF Correction See all GeneRIFs (71)

Variation

Go to the top of the page Help

Alleles

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

Gene trapped (1)
Targeted (5) 1 citation
Endonuclease-mediated (10) 1 citation

General gene information

Go to the top of the page Help

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables 14-3-3 protein binding	IBA Inferred from Biological aspect of Ancestor more info
enables 14-3-3 protein binding	IDA Inferred from Direct Assay more info	PubMed

Process	Evidence Code	Pubs
involved_in apoptotic process	IBA Inferred from Biological aspect of Ancestor more info
involved_in brain development	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within cellular response to dexamethasone stimulus	IDA Inferred from Direct Assay more info	PubMed
involved_in defense response to virus	ISO Inferred from Sequence Orthology more info
involved_in intracellular signal transduction	ISO Inferred from Sequence Orthology more info
involved_in intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in negative regulation of TOR signaling	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within negative regulation of TOR signaling	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in negative regulation of TOR signaling	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within negative regulation of glycolytic process	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in negative regulation of signal transduction	IEA Inferred from Electronic Annotation more info
involved_in neuron differentiation	ISO Inferred from Sequence Orthology more info
involved_in neuron migration	ISO Inferred from Sequence Orthology more info
involved_in neurotrophin TRK receptor signaling pathway	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within protein-containing complex disassembly	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within reactive oxygen species metabolic process	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in response to hypoxia	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within response to hypoxia	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in response to hypoxia	ISO Inferred from Sequence Orthology more info

Component	Evidence Code	Pubs
located_in cytoplasm	ISO Inferred from Sequence Orthology more info
located_in cytosol	ISO Inferred from Sequence Orthology more info
located_in mitochondrion	IDA Inferred from Direct Assay more info	PubMed

General protein information

Go to the top of the page Help

Preferred Names: DNA damage-inducible transcript 4 protein

Names: HIF-1 responsive RTP801; HIF-1 responsive protein RTP801; REDD-1; dexamethasone-induced gene 2 protein; protein regulated in development and DNA damage response 1

NCBI Reference Sequences (RefSeq)

Go to the top of the page Help

NEW Try the new Transcript table

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.