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ZIC1 encodes a member of the ZIC family of C2H2-type zinc finger proteins. Additionally we are shipping ZIC1 Antibodies (78) and many more products for this protein.
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Two proposed mechanisms for Zic-mediated cerebellar developmental control have been documented: regulation of neuronal progenitor proliferation-differentiation and the patterning of the cerebellar primordium. Clinical studies have also revealed that ZIC1 gain of function mutations contribute to coronal craniosynostosis, a rare skull malformation.
By unbiased genome-wide DNA methylation (show HELLS Proteins) profiling and comprehensive stepwise verification and validation studies using in vitro and patient-derived samples, we identified 3 promising methylation markers (GHSR (show GHSR Proteins), SST (show SST Proteins), and ZIC1) associated with a 3q gain for the detection of cervical (pre)cancer
down-regulated expression of ZIC1 contributed to the inhibition of cell proliferation, and inhibited the growth of tumor
our results suggest that the Zic1 promoter methylation rate in plasma-derived DNA is of great significance for the early screening of gastric cancer and monitoring of tumorigenesis
Gain-of-Function Mutations in ZIC1 Are Associated with Coronal Craniosynostosis and Learning Disability.
ZIC1 might play a role in the development of Ovarian Cancer, and may be a therapeutic target in OC.
aberrant methylation is an important mechanism for ZIC1 inactivation in Hepatocellular carcinoma (HCC (show FAM126A Proteins)).
ZIC1 is frequently inactivated by promoter hypermethyaltion and functions as a tumor suppressor in thyroid cancer through modulating PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) and MAPK (show MAPK1 Proteins) signaling pathways and transcription factor FOXO3a (show FOXO3 Proteins).
Loss of ZIC1 expression is associated with malignant pleural mesothelioma.
Methylation of ZIC1, a putative tumor suppressor, may be a novel determinant of ovarian cancer outcome
snai2 and sox10 (show SOX10 Proteins) expression was severely impaired upon manipulation of Znf703 (show ZNF703 Proteins) expression levels in the embryo suggesting that Znf703 (show ZNF703 Proteins) participates in neural crest formation downstream of Pax3 (show PAX3 Proteins) and Zic1 in Xenopus
Zic1, expressed at the anterior neural plate, is necessary and sufficient to promote placode fate.
Pax3 (show PAX3 Proteins) and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers.
Pax3 (show PAX3 Proteins) and Zic1 drive induction and differentiation of multipotent, migratory, and functional neural crest in Xenopus embryos.
XMeis3 (show MEIS3 Proteins) protein knock down also causes a loss of primary neuron and neural crest cell lineages, without altering expression of Zic, Sox (show PIPOX Proteins) or Pax3 (show PAX3 Proteins) genes.
Co-activation of Pax3 (show PAX3 Proteins) and Zic1, in concert with Wnt (show WNT2 Proteins), plays a decisive role for early neural crest determination in the correct place of the Xenopus ectoderm.
These data suggest that interruption of BMP signaling facilitates neural determination via a complex mechanism, involving multiple regulatory factors that cooperate to control zic1 expression
Zic1 directly upregulated the Xfeb gene during early neural development.
Zic1 is an activator of Wnt (show WNT2 Proteins) signaling.
Data show that Pax3 (show PAX3 Proteins) and Zic1 are necessary and sufficient to promote hatching gland and preplacodal fates, respectively, and that their combined activity is essential to specify the neural crest.
Geminin (show GMNN Proteins) and Zic1 could cooperatively activate the expression of several shared targets encoding transcription factors that control neurogenesis, neural plate patterning, and neuronal differentiation.
Zic1 and Zic2 (show ZIC2 Proteins) proteins are essential to control the balance between two defined neuron types in the postnatal forebrain.
Brn2 (show POU3F2 Proteins)-Zic1 axis is essential to specify neural fate in retinoic-acid-treated embryonic stem cells.
Zic1 and Zic2 (show ZIC2 Proteins) are required for coordinating mature neuronal gene expression patterns.
Association with DNA-bound Pax3 (show PAX3 Proteins) strengthens the ability of both Zic1 and Gli2 to transactivate Myf5 (show MYF5 Proteins) in the epaxial somite.
Zic1 and Zic4 (show ZIC4 Proteins) have both Shh (show SHH Proteins)-dependent and -independent roles during cerebellar development and multiple developmental disruptions underlie Zic1/4-related Dandy-walker malformation.
Myf5 (show MYF5 Proteins) activation in newly forming somites is delayed in Zic2 (show ZIC2 Proteins) mutant embryos until the time of Zic1 activation, and both Zic2 (show ZIC2 Proteins) and Myf5 (show MYF5 Proteins) require noggin (show NOG Proteins) for their activation
Zic1, a neural developmental transcription factor, plays an important role in shear flow mechanotransduction in osteocytes.
findings suggest that Zic1 controls the expansion of neuronal precursors by inhibiting the progression of neuronal differentiation
The functions of Zic1 and Zic3 (show ZIC3 Proteins) may be essential to increasing neural cell numbers regionally in the medial telencephalon and to proper mediolateral patterning of the telencephalon.
This gene encodes a member of the ZIC family of C2H2-type zinc finger proteins. Members of this family are important during development. Aberrant expression of this gene is seen in medulloblastoma, a childhood brain tumor. This gene is closely linked to the gene encoding zinc finger protein of the cerebellum 4, a related family member on chromosome 3. This gene encodes a transcription factor that can bind and transactivate the apolipoprotein E gene.
Zic family member 1 (odd-paired homolog, Drosophila)
, Zinc finger protein of the cerebellum 1
, zinc finger protein 201
, zinc finger protein ZIC 1
, zic protein member 1
, zinc finger protein of the cerebellum 1
, ZIC-related protein 1
, Zic family member 1 (odd-paired homolog)
, odd-paired homolog