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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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our findings demonstrate that Myt1L is an essential regulator of oligodendrocyte precursor cell differentiation
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.
(1) MYT1L is required for neuronal differentiation and identified ID1 (show ID1 Antibodies) as a target. (2) Although MYT1L prevented expression of ID1 (show ID1 Antibodies), it induced expression of a large number of terminal differentiation genes. (3) Consistently, expression of MYT1L in the human brain coincided with neuronal maturation and inversely correlated with that of ID1 (show ID1 Antibodies) and ID3 (show ID3 Antibodies) throughout the lifespan.
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.
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 factor 1
, neural zinc finger protein NZF-1
, neural zinc finger transcription factor 1
, postmeiotic neural gene 1
, postmitotic neural gene 1 protein
, zinc finger protein Png-1