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suggest that NFIX plays a role in regulating progenitor cell biology within the embryonic and post-natal cerebellum, as well as an ongoing role within multiple neuronal and glial populations within the adult cerebellum
Under basal conditions, adult hippocampal neural stem cells (AH-NSCs) generate neurons and astrocytes, but not oligodendrocytes. The factors limiting oligodendrocyte production, however, remain unclear. Here, we reveal that the transcription factor NFIX plays a key role in this process.
These data demonstrate functional cooperation between Sox6 and Nfix in regulating MyHC-I (show MYH7 Proteins) expression during prenatal muscle development.
Nfix deficiency delays intermediate progenitor cell production and prolongs the neurogenic window, resulting in an increased number of neurons in the postnatal forebrain.
Nfix is required for maintaining muscle physiology postnatally and for the proper timing of muscle regeneration.
The data indicate that NFIX influences the lineage specification of postnatal subventricular zone neural stem cells, specifically suppressing oligodendrogenesis.
The ependymal layer of the lateral ventricles was frequently absent in Nfix(-/-) mice
NFIX acts as a regulator of lineage specification in the haematopoietic system.
NFIX plays a central role in hippocampal morphogenesis, regulating the formation of neuronal and glial populations within this
Bbx (show BBX Proteins) is a downstream target of NFIX during development of the forebrain.
Compared to noncancerous esophageal mucosa, miR (show MLXIP Proteins)-1290 expression was upregulated, while NFIX mRNA expression was downregulated in ESCC tissues. Data suggest that the dysregulation of miR (show MLXIP Proteins)-1290-NFIX axis may play crucial roles in esophageal carcinogenesis and progression.
A novel de novo pathogenic variant in the NFIX gene identified in a case of Marshall-Smith syndrome with precocious puberty and aortic root dilatation.
Plasma miR (show MLXIP Proteins)-1914* and -1915 interact with NFIX RNA.
Report novel mutations of NFIX gene causing Marshall-Smith syndrome or Sotos-like syndrome.
miR (show MLXIP Proteins)-1290 functions as a tumor oncogene (show RAB1A Proteins) in the progression of esophageal squamous cell carcinoma by targeting NFIX
NFIX analysis should be considered in patients presenting with overgrowth, macrocephaly and developmental delay including those in whom Sotos syndrome has been considered clinically but are negative for pathogenic NSD1 variants.
TGF-beta (show TGFB1 Proteins)-mediated suppression of ANT2 (show SLC25A5 Proteins) through NF1 (show NF1 Proteins)/Smad4 (show SMAD4 Proteins) complexes contributes to oxidative stress and DNA damage during induction of cellular senescence.
Deletions in the 3' part of the NFIX gene including a recurrent Alu-mediated deletion of exon 6 and 7 account for previously unexplained cases of Marshall-Smith syndrome.
missense mutations in NFIX were able to cause Sotos-like features.
DNA methylation (show HELLS Proteins) shows genome-wide association of NFIX, RAPGEF2 (show RAPGEF2 Proteins) and MSRB3 (show MSRB3 Proteins) with gestational age at birth.
NFIX had highest expression in brain; medial expression in lung and muscle; and lower expression in spleen, kidney, liver and heart of both embryo and adult cattle. However, expression levels in adult tissues were significantly decreased.
Two sequence variants of the Nfix gene are significantly associated with growth traits at different ages.
The protein encoded by this gene is a transcription factor that binds the palindromic sequence 5'-TTGGCNNNNNGCCAA-3 in viral and cellular promoters. The encoded protein can also stimulate adenovirus replication in vitro. Three transcript variants encoding different isoforms have been found for this gene.
CCAAT-box-binding transcription factor
, TGGCA-binding protein
, nuclear factor 1 X-type
, nuclear factor 1/X
, NF1-X1 protein
, nuclear factor I-X protein
, Nuclear factor 1/X