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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
These results suggesta potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination.
UVA-induced caspase-3 (zeige CASP3 Proteine) cleavage and DNA fragmentation were suppressed by the knockdown of human Myt1 in skin cancer cells.
we show that Ascl1 (zeige ASCL1 Proteine) induces the transcription factor MyT1 while promoting neuronal differentiation...It promotes neuronal differentiation by counteracting the inhibitory activity of Notch (zeige NOTCH1 Proteine) signaling at multiple levels, targeting the Notch1 (zeige NOTCH1 Proteine) 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 (zeige KDM1A Proteine) 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 (zeige SIN3B Proteine). Depending on the relative availability of Sin3B (zeige SIN3B Proteine) isoforms, the Myt1 gene family may favor the silencing of genes during neural development.
Myt1, Myt3, and Ngn3 (zeige NEUROG3 Proteine) are induced by Mfng (zeige MFNG Proteine) and have roles in Mfng (zeige MFNG Proteine)-mediated repression of Notch (zeige NOTCH1 Proteine) signaling which could serve as a trigger for endocrine islet differentiation
These findings suggest Myt1 is involved in proper endocrine differentiation and function.
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