DDIT4L

DNA-damage-inducible transcript 4 like (DDIT4L) or regulated in development and DNA damage response 2 (REDD2) is a protein that in humans is encoded by the DDIT4L gene.^[5][6] The gene is located on chromosome 4 or chromosome 3 in human or mouse respectively.^[7][8]

DDIT4L
Identifiers
Aliases	DDIT4L, REDD2, Rtp801L, DNA damage inducible transcript 4 like
External IDs	OMIM: 607730; MGI: 1920534; HomoloGene: 12698; GeneCards: DDIT4L; OMA:DDIT4L - orthologs
Gene location (Human) Chr. Chromosome 4 (human)[1] Band 4q24 Start 100,185,870 bp[1] End 100,190,782 bp[1]
Gene location (Mouse) Chr. Chromosome 3 (mouse)[2] Band 3|3 G3 Start 137,327,373 bp[2] End 137,334,094 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in deltoid muscle tibialis anterior muscle quadriceps femoris muscle vastus lateralis muscle Skeletal muscle tissue of biceps brachii Skeletal muscle tissue of rectus abdominis gastrocnemius muscle muscle of thigh cartilage tissue body of tongue Top expressed in temporal muscle sternocleidomastoid muscle extraocular muscle triceps brachii muscle masseter muscle quadriceps femoris muscle digastric muscle gastrocnemius muscle medial head of gastrocnemius muscle vastus lateralis muscle More reference expression data BioGPS n/a
Gene ontology Molecular function protein binding Cellular component cytoplasm Biological process negative regulation of signal transduction Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 115265 73284 Ensembl ENSG00000145358 ENSMUSG00000046818 UniProt Q96D03 Q8VHZ5 RefSeq (mRNA) NM_145244 NM_030143 RefSeq (protein) NP_660287 NP_084419 Location (UCSC) Chr 4: 100.19 – 100.19 Mb Chr 3: 137.33 – 137.33 Mb PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Function

DDIT4L is a negative regulator of mTOR.^[9] DDIT4L is a stress responsive protein, its expression is increased under the hypoxic condition and causes or sensitize towards cell death through the regulation mTOR activity and reduction of thioredoxin-1.^[10][11][12] Cardiomyocytes showed increase expression of DDIT4L under pathological stress, which promoted autophagy through the inhibition of mTORC1, not mTORC2.^[11]

Role in Disease

In fibrosis, nuclear long noncoding RNA (lncRNA) H19X repressed DDIT4L gene expression, specifically interacting with a region upstream of the DDIT4L gene and increased collagen expression and fibrosis.^[13] Expression of DDIT4L is increased in pathological cardiac hypertrophy but not in those of physiological cardiac hypertrophy. Such mice had mild systolic dysfunction, increased baseline autophagy, reduced mTORC1 activity, and increased mTORC2 activity.^[11]

See also

• DDIT4/ REDD1
• mTOR
• mTORC1
• mTORC2