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Our preliminary results identified risk variants of GLI3 that are associated with NSCL (zeige NHLH1 Proteine)/P susceptibility in a Chinese population. In particular, rs3801161 and its haplotypes rs3801161-rs7785287 displayed significant association with NSCL (zeige NHLH1 Proteine)/P and survived Bonferroni correction for multiple comparisons.
A novel GLI3 missense variant in a family that caused a spectrum of digital anomalies. All affected individuals that were tested harbored a c.1826G>A (p.(Cys609Tyr)) variant in GLI3. Functional studies of the murine p.Cys609Tyr GLI3 showed that the mutant protein is not efficiently processed to GLI3R, resulting in a full-length protein with basal transcriptional activity and submaximal pathway activation.
Hedgehog (zeige SHH Proteine) pathway dysregulation contributes to the pathogenesis of human gastrointestinal stromal tumors via GLI (zeige GLI1 Proteine)-mediated activation of KIT expression.
The c.480dupC of the GLI3 gene probably underlies the synpolydactyly in this family.
Methylation at K436 and K595 respectively by Set7 (zeige SETD7 Proteine) increases the stability and DNA binding ability of Gli3, resulting in an enhancement of Shh (zeige SHH Proteine) signaling activation.
Data suggest that negative feedback mediated by GLI3 (GLI (zeige GLI1 Proteine)-Kruppel family member) acts to finely tune SHH (sonic hedgehog (zeige SHH Proteine)) signaling. During medulloblastoma (MB) formation, nerve tissue cells appear to express nestin (zeige NES Proteine) which hyperactivates SHH (zeige SHH Proteine) signaling by abolishing negative feedback by GLI3. Restoration of intrinsic negative feedback by repressing nestin (zeige NES Proteine) expression represents a promising approach to treat MB. [REVIEW]
the first report of the assessment of the frequency of GLI3/SHH (zeige SHH Proteine)/preZRS/ZRS in Chinese polydactyly patients to show any higher possibility of mutations or variants for the 4 genes or sequences in China
Gli3 and Teashirt3 (zeige ZNF537 Proteine) might play an important role in the normal development of the ureter.
a novel GLI3 mutation c.714T>A (p.Y238*) was identified in a Chinese family with pre-axial polydactyly. Our results broadened the phenotypic spectrum of GLI3 mutations and demonstrated the feasibility of WES in clinical application of molecular diagnosis.
we describe an ~5 kb deletion within the SHH (zeige SHH Proteine) repressor GLI3 in two patients with bilateral tibial hemimelia. This deletion results in a truncated GLI3 protein that lacks a DNA-binding domain and cannot repress hedgehog (zeige SHH Proteine) signaling.
Gli3 activity in mouse thymic epithelial cells (TECs) promotes positive selection and differentiation from CD4 (zeige CD4 Proteine)(+) CD8 (zeige CD8A Proteine)(+) to CD4 (zeige CD4 Proteine)(+) CD8 (zeige CD8A Proteine)(-) single-positive (SP4) cells in the fetal thymus and Gli3 represses Shh (zeige SHH Proteine) constitutive deletion of Gli3, and conditional deletion of Gli3 from TECs, reduced differentiation to SP4, whereas conditional deletion of Gli3 from thymocytes did not.
loss of Spop (zeige SPOP Proteine), but not Spopl (zeige SPOPL Proteine), disrupts chondrocyte hypertrophy and osteoblast differentiation in the mouse, suggesting the requirement for Spop (zeige SPOP Proteine)-mediated protein degradation in mouse skeletal development; overexpressed Spop (zeige SPOP Proteine) targets both Gli3FL and Gli3R for ubiquitination and degradation and Spop (zeige SPOP Proteine) is an important positive regulator of Ihh (zeige IHH Proteine) signaling and skeletal development
mutual interactions between Gli3, Wnt8b, and Fgf17 (zeige FGF17 Proteine) are crucial elements of the balance between these factors thereby conferring robustness to the patterning process
Results demonstrate a negative role of Spop (zeige SPOP Proteine) in the level and activity of Gli3, Shh (zeige SHH Proteine) signaling and ventral spinal cord patterning.
Gli2 and Gli3 are dephosphorylated and activated in cilia and that impaired Gli2 and Gli3 processing in Ta3 (zeige HSP90B1 Proteine) mutant is at least in part due to a decrease in Gli2 and Gli3 phosphorylation.
These results suggest that Tctn1 (zeige TCTN1 Proteine), Tctn2 (zeige TCTN2 Proteine), and Tctn3 (zeige TCTN3 Proteine) are functionally divergent with respect to their role in ciliogenesis and Hedgehog (zeige SHH Proteine) signaling but conserved in neural tube patterning and Gli3 processing.
Results indicate that the transcription factor Gli3 (Gli3)-mutant fetal liver (FL) had increased sonic hedgehog (Shh (zeige SHH Proteine)) signaling resulting in decreased B cell development.
Our findings show how Nestin (zeige NES Proteine) drives hedgehog (zeige SHH Proteine) pathway-driven cancers and the tumor-promoting effects of Nestin (zeige NES Proteine) were mediated by binding to Gli3, a zinc finger transcription factor (zeige OSR1 Proteine) that negatively regulates hedgehog (zeige SHH Proteine) signaling.
Gli3 gene is a direct target for repression by Tgifs during the neural tube patterning.
Sufu (zeige SUFUH Proteine) is upregulated in active Shh (zeige SHH Proteine) responding tissues and accompanies Gli (zeige GLI1 Proteine) activators translocating into and Gli (zeige GLI1 Proteine) repressors out of the nucleus.
Zebrafish Gli3 functions as both an activator and a repressor in Hedgehog (zeige SHH Proteine) signaling. In the eye, Gli3 is also required for proper ath5 (zeige ATOH7 Proteine) expression and the differentiation of retinal ganglion cells.
The results provided evidence that polymorphisms in the GLI3 gene are associated with growth traits, and may be used for marker-assisted selection in beef cattle breeding program.
This gene encodes a protein which belongs to the C2H2-type zinc finger proteins subclass of the Gli family. They are characterized as DNA-binding transcription factors and are mediators of Sonic hedgehog (Shh) signaling. The protein encoded by this gene localizes in the cytoplasm and activates patched Drosophila homolog (PTCH) gene expression. It is also thought to play a role during embryogenesis. Mutations in this gene have been associated with several diseases, including Greig cephalopolysyndactyly syndrome, Pallister-Hall syndrome, preaxial polydactyly type IV, and postaxial polydactyly types A1 and B.
GLI-Kruppel family member GLI3
, glioma-associated oncogene family zinc finger 3
, oncogene GLI3
, transcriptional activator GLI3
, zinc finger protein GLI3
, GLI-Kruppel family member GLI3 (Greig cephalopolysyndactyly syndrome)
, GLI3 full length protein
, neural specific DNA binding protein
, neural-specific DNA-binding protein xGLI3
, GLI-Kruppel family member 3
, GLI3 form of 190 kDa
, anterior digit pattern deformity
, extra toes
, polydactyly Nagoya
, zinc finger transcription factor Gli3
, GLI family zinc finger 3