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binds specifically to retinoic acid response elements and acts as a transcriptional activator; may regulate gene expression in the nervous system and pituitary. Additionally we are shipping and and many more products for this protein.
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This study demonstrates that MYT1L variants are associated with syndromic obesity in humans. The mechanism is related to dysregulated expression of neurodevelopmental genes and altered development of the neuroendocrine hypothalamus
Haplotype-dependent allele-specific methylation of MYT1L gene is associated with neurological disorders.
Our data strongly strengthen the hypothesis that MYT1L is the causal gene for the observed syndromal intellectual disability.
MYT1L rs17039396 variants are associated with clinical outcome in gastric cancer.
MYT1L and the SNTG2 (show SNTG2 Antibodies) genes within the reported region could probably relate to the phenotypic discordance of the monozygotic twins.
Data indicate that reintroduction of A2BP1 (show A2BP1 Antibodies) or Myt1L in glioblastoma multiforme (GBM) cell lines and glioma stem cells profoundly inhibited tumorigenesis.
A meta-analysis of four recently published studies that together provide strong evidence for an association between variably sized microduplications involving the MYT1L gene and schizophrenia.
Results from this study indicate that the 2p25.3 duplication disrupting PXDN (show PXDN Antibodies) and MYT1L is a potential autism-causing variant in the pedigree reported here and should receive further consideration as a candidate for autism
Findings suggest that MYT1L may represent a susceptibility gene for schizophrenia in the Han Chinese population and show that a specific SNP may increase susceptibility in females.
MYT1L deletion gives a nonspecific clinical phenotype shared by patients with 2p25.3 deletions, with only intellectual disability and obesity/overweight being present in all patients.
Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity.
NZF-1 was expressed later in post-mitotic neurons. NZF-2 was initially expressed in neuronal cells a little earlier than NZF-3. NZF-3 was initially expressed in neuronal cells, just after proliferation was complete.
binds specifically to retinoic acid response elements and acts as a transcriptional activator; may regulate gene expression in the nervous system and pituitary
, myelin transcription factor 1-like protein
, neural zinc finger transcription factor 1
, neural zinc finger factor 1
, neural zinc finger protein NZF-1
, postmeiotic neural gene 1
, postmitotic neural gene 1 protein
, zinc finger protein Png-1