Редактирование: DLX2

Homeobox protein DLX-2

==Publications==

{{medline-entry
|title=A gain-of-function senescence bypass screen identifies the homeobox transcription factor [[DLX2]] as a regulator of [[ATM]]-p53 signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26833729
|abstract=Senescence stimuli activate multiple tumor suppressor pathways to initiate cycle arrest and a differentiation program characteristic of senescent cells. We performed a two-stage, gain-of-function screen to select for the genes whose enhanced expression can bypass replicative senescence. We uncovered multiple genes known to be involved in p53 and Rb regulation and [[ATM]] regulation, two components of the CST (CTC1-[[STN1]]-TEN1) complex involved in preventing telomere erosion, and genes such as [[REST]] and [[FOXO4]] that have been implicated in aging. Among the new genes now implicated in senescence, we identified [[DLX2]], a homeobox transcription factor that has been shown to be required for tumor growth and metastasis and is associated with poor cancer prognosis. Growth analysis showed that [[DLX2]] expression led to increased cellular replicative life span. Our data suggest that [[DLX2]] expression reduces the protein components of the TTI1/TTI2/TEL2 complex, a key complex required for the proper folding and stabilization of [[ATM]] and other members of the PIKK (phosphatidylinositol 3-kinase-related kinase) family kinase, leading to reduced [[ATM]]-p53 signaling and senescence bypass. We also found that the overexpression of [[DLX2]] exhibited a mutually exclusive relationship with p53 alterations in cancer patients. Our functional screen identified novel players that may promote tumorigenesis by regulating the [[ATM]]-p53 pathway and senescence. 
|mesh-terms=* Ataxia Telangiectasia Mutated Proteins
* Cell Line
* Cellular Senescence
* Computational Biology
* Gene Expression Regulation
* Homeodomain Proteins
* Humans
* Reproducibility of Results
* Signal Transduction
* Telomere Homeostasis
* Transcription Factors
* Transcriptional Activation
* Tumor Suppressor Protein p53
|keywords=* ATM
* genetic screen
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4743059
}}