Symbol
| DDIT3
| contributors: npt/shn - updated : 08-06-2015
|
HGNC name
| DNA-damage-inducible transcript 3
|
HGNC id
| 2726
|
corresponding disease(s)
|
DDIT3
|
Other morbid association(s)
|
Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
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tumoral
|  
| translocation
|  
|  
|
translocated with FUS in t(12;16)(q13;p11) and with ESWR1 in t(12;22)(q13;q12) in myxoid liposarcoma | constitutional
|  
|  
|  
| loss of function
|
in conjunction with a COMP mutation, may lead to aggravation of the skeletal phenotype via a potentially synergistic effect on endochondral ossification | |
Variant & Polymorphism
|
| |
Candidate gene
Marker
Therapy target
|
System | Type | Disorder | Pubmed |
diabete | | | |
therapeutic potential of CHOP inhibition in the management of diabetic cardiovascular complications including diabetic cardiomyopathy | digestive | liver | | |
targeting DDIT3/ERO1A signalling could be a novel therapeutic approach during acute liver failure (ALF) |
| | | |
| Chop-null mice are resistant to fibrosis, which is a key risk factor for hepatocellular carcinoma (HCC) |