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wide analyses of the effects of Myt1 and Myt1l expression in a glioblastoma cell line suggest that the two proteins have largely similar effects on endogenous gene expression. Transcriptional repression is likely mediated by binding to DNA via the known consensus site, whereas this site is not associated with the transcriptional start sites of genes with higher expression in the presence of Myt1 or Myt1l.
A novel missense variant affecting function, c.323C>T (p.(Ser108Leu)), was identified in MYT1, in a patient presenting with a severe form of OAVS. MYT1 overexpression downregulated all RA receptors genes in vitro.
although depletion of MYT1 alone did not affect long-term cell growth, it potentiated with DNA damage to inhibit cell growth in clonogenic survival and tumor xenograft models
present in brain in infancy and prenatally in infants with periventricular leukomalacia
These results suggesta potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination.
UVA-induced caspase-3 cleavage and DNA fragmentation were suppressed by the knockdown of human Myt1 in skin cancer cells.
we show that Ascl1 induces the transcription factor MyT1 while promoting neuronal differentiation...It promotes neuronal differentiation by counteracting the inhibitory activity of Notch signaling at multiple levels, targeting the Notch1 receptor and many of its downstream targets
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.
MyT1 is a subunit of the neural cell type-specific LSD1 complex.
used NMR spectroscopy, in combination with surface plasmon resonance and data-driven molecular docking, to delineate the mechanism of DNA binding for double zinc finger polypeptides derived from MyT1
These results suggest a potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination.
in embryonic mouse nervous system, the expression of NZF-2b starts as early as at 9.5 days post-coitum (dpc) in newly differentiated neurons in the central nervous system (CNS) and the peripheral nervous system (PNS)
Expression of Myt1 inhibited the differentiation of progenitors into oligodendrocytes as assessed by morphology, immunostaining, and myelin gene expression. Progenitor differentiation was similarly inhibited by expression of Myt1.
The Myt1 family of zinc finger proteins, when bound to a neural promoter, can recruit Sin3B. Depending on the relative availability of Sin3B isoforms, the Myt1 gene family may favor the silencing of genes during neural development.
Myt1, Myt3, and Ngn3 are induced by Mfng and have roles in Mfng-mediated repression of Notch signaling which could serve as a trigger for endocrine islet differentiation
These findings suggest Myt1 is involved in proper endocrine differentiation and function.
MyT1 ZnFs recognize the major groove of DNA in a way that appears to differ from other known zinc binding domains.
Myt1 and Ngn3 form a feed-forward expression loop to promote endocrine islet cell differentiation.
The protein encoded by this gene is a member of a family of neural specific, zinc finger-containing DNA-binding proteins. The protein binds to the promoter regions of proteolipid proteins of the central nervous system and plays a role in the developing nervous system.
myelin transcription factor 1
, myelin transcription factor I
, proteolipid protein binding protein
, proteolipid protein-binding protein
, neural zinc finger factor 2
, neural zinc finger transcription factor 2