Liver carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
HCC cells with higher DLX2 expression were more sensitive to acRoots.
|
30415058 |
2019 |
Brain Diseases
|
0.010 |
AlteredExpression
|
group |
BEFREE |
DLX1 and/or DLX2 activated the transcription of both <i>Gad</i> genes, and defects in <i>Dlx</i> function disrupted the differentiation of GABAergic interneurons with global reduction in GABA levels in the forebrains of the <i>Dlx1/Dlx2</i> double knock-out mouse <i>in vivo</i> Identification of <i>Gad</i> genes as direct <i>Dlx</i> transcriptional targets is significant; it extends our understanding of <i>Dlx</i> gene function in the developing forebrain beyond the regulation of tangential interneuron migration to the differentiation of GABAergic interneurons arising from the basal telencephalon, and may help to unravel the pathogenesis of several developmental brain disorders.<b>SIGNIFICANCE STATEMENT</b> GABA is the major inhibitory neurotransmitter in the brain.
|
28821666 |
2017 |
Dental Fluorosis, Acquired
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Our results provided evidence that polymorphisms in TIMP1, DLX1 and DLX2 genes may be associated with DF phenotypes.
|
28131910 |
2017 |
Tooth Abnormalities
|
0.010 |
Biomarker
|
group |
BEFREE |
The Dlx2‑overexpressed mice exhibited tooth abnormalities including incisor cross‑bite, shortened tooth roots, increased cementum deposition, periodontal ligament disorganization and osteoporotic alveolar bone.
|
28447749 |
2017 |
Tumor Initiation
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
We show that p53-R273H-mediated DLX2 repression leads to upregulation of Neuropilin-2 (NRP2), a multifunctional co-receptor involved in tumor initiation, growth, survival and metastasis. p53-R273H-induced cell mobility is effectively suppressed by DLX2 expression.
|
28796261 |
2017 |
Tumor Cell Invasion
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
In this study, we demonstrate that the hotspot mutation, p53-R273H, promotes cell migration, invasion in vitro and tumor metastasis in vivo. p53-R273H significantly represses expression of DLX2, a homeobox protein involved in cell proliferation and pattern formation.
|
28796261 |
2017 |
Secondary Neoplasm
|
0.010 |
GeneticVariation
|
group |
BEFREE |
Together, these results reveal an important role for DLX2-NRP2 in p53-R273H-induced cell mobility and tumor metastasis.
|
28796261 |
2017 |
Dental fluorosis
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Our results provided evidence that polymorphisms in TIMP1, DLX1 and DLX2 genes may be associated with DF phenotypes.
|
28131910 |
2017 |
Hematologic Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
The distal-less homeobox2 (DLX2) gene encodes for a homeobox transcription factor involved in morphogenesis and its deregulation was found in human solid tumors and hematologic malignancies.
|
26799321 |
2016 |
Lymphoproliferative Disorders
|
0.010 |
AlteredExpression
|
group |
BEFREE |
TRAF1 is amongst the most highly TES1-induced target genes and is abundantly expressed in EBV-associated lymphoproliferative disorders.
|
25996949 |
2015 |
Mental Retardation
|
0.010 |
Biomarker
|
disease |
BEFREE |
The 2q31.1 deletion resulted in the loss of one copy of several known disease genes, including GAD1, DCAF17, SLC25A12 and ITGA6 associated with mental retardation and facial abnormalities and DLX1/DLX2 partially associated with limb abnormalities.
|
24412318 |
2014 |
Deformity of limb
|
0.010 |
Biomarker
|
group |
BEFREE |
The 2q31.1 deletion resulted in the loss of one copy of several known disease genes, including GAD1, DCAF17, SLC25A12 and ITGA6 associated with mental retardation and facial abnormalities and DLX1/DLX2 partially associated with limb abnormalities.
|
24412318 |
2014 |
Intellectual Disability
|
0.010 |
Biomarker
|
group |
BEFREE |
The 2q31.1 deletion resulted in the loss of one copy of several known disease genes, including GAD1, DCAF17, SLC25A12 and ITGA6 associated with mental retardation and facial abnormalities and DLX1/DLX2 partially associated with limb abnormalities.
|
24412318 |
2014 |
Glioblastoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Upregulation of DLX2 confers a poor prognosis in glioblastoma patients by inducing a proliferative phenotype.
|
23331016 |
2013 |
Adult Glioblastoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Upregulation of DLX2 confers a poor prognosis in glioblastoma patients by inducing a proliferative phenotype.
|
23331016 |
2013 |
Childhood Glioblastoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Upregulation of DLX2 confers a poor prognosis in glioblastoma patients by inducing a proliferative phenotype.
|
23331016 |
2013 |
Glioblastoma Multiforme
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Collectively, these data identified high expression of DLX2 as a poor prognostic marker to GBM patients.
|
23331016 |
2013 |
Malignant neoplasm of breast
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our studies indicate that DLX genes are involved in human breast cancer progression, and that DLX2 and DLX5 genes might serve as prognostic markers.
|
21108812 |
2010 |
Secondary malignant neoplasm of lung
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Instead, in bone and lung metastases resulting from intravenous injection we detected expression of DLX5/6 but not of DLX2, suggesting that DLX5/6 are activated during metastasis formation, and that their expression is alternative to that of DLX2.
|
21108812 |
2010 |
Breast Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Our studies indicate that DLX genes are involved in human breast cancer progression, and that DLX2 and DLX5 genes might serve as prognostic markers.
|
21108812 |
2010 |
Autism Spectrum Disorders
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
The DLX1and DLX2 genes and susceptibility to autism spectrum disorders.
|
18728693 |
2009 |
Epilepsy
|
0.010 |
Biomarker
|
disease |
BEFREE |
As a strategy to define the embryonic origin and neurochemical phenotype of cells in this disease, we probed specimens (n = 10) resected during epilepsy surgery with a panel of 13 antibodies recognizing proteins associated with (i) specific progenitor cell types including brain lipid binding protein (BLBP), collapsin response mediator protein 4 (CRMP4), Dlx1, Dlx2, GFAPdelta, MASH1, Otx1, Pax6, vimentin and phosphorylated vimentin and (ii) excitatory or inhibitory neurochemical phenotypes such as the vesicular glutamate transporters-1 and 2 (VGLUT-1, VGLUT-2), or the vesicular GABA transporter (VGAT).
|
17711980 |
2007 |
Rieger syndrome
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
This mutation is associated with iris hypoplasia (IH); in contrast a Rieger syndrome mutation, PITX2 T68P, which presents clinically with the full spectrum of developmental anomalies (including tooth anomalies), is unable to transactivate the Dlx2 promoter.
|
11929847 |
2002 |
Hypoplasia of iris
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Since Dlx2 expression is required for tooth and craniofacial development the lack of tooth anomalies in the patient with IH may be due to the residual activity of this mutant in activating the Dlx2 promoter.
|
11929847 |
2002 |
Axenfeld-Rieger syndrome
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
This mutation is associated with iris hypoplasia (IH); in contrast a Rieger syndrome mutation, PITX2 T68P, which presents clinically with the full spectrum of developmental anomalies (including tooth anomalies), is unable to transactivate the Dlx2 promoter.
|
11929847 |
2002 |