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Human Polyclonal MLZE Primary Antibody for ICC, IF - ABIN6579175
Betancourt, Katzman, Chen: Nuclear factor one B regulates neural stem cell differentiation and axonal projection of corticofugal neurons. in The Journal of comparative neurology 2014
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Human Polyclonal MLZE Primary Antibody for IHC, IHC (p) - ABIN4339338
Taglietti, Maroli, Cermenati, Monteverde, Ferrante, Rossi, Cossu, Beltrame, Messina: Nfix Induces a Switch in Sox6 Transcriptional Activity to Regulate MyHC-I Expression in Fetal Muscle. in Cell reports 2016
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Human Polyclonal MLZE Primary Antibody for WB - ABIN4339337
Piper, Gronostajski, Messina: Nuclear Factor One X in Development and Disease. in Trends in cell biology 2019
Mice lacking Nfix exhibit reduced numbers of granule cell precursors during early postnatal development, but elevated numbers of these cells at postnatal day 15. Moreover, Nfix(-/-) GNPs exhibit increased proliferation when cultured in vitro, suggestive of a role for NFIX in promoting GNP differentiation.
By modelling brain structure and behavior in Nfix heterozygous mice, the study provides a significant conceptual advance in our understanding of the factors underlying Malan syndrome.
Nfix is regulated through the RhoA/ROCK axis, which maintains embryonic myogenesis.
This study reveal Foxj1, a key factor promoting ependymal cell maturation, as a target for NFIX-mediated transcriptional activation.
overexpression in dystrophic muscles increases regeneration and markedly exacerbates the pathology
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 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.
Findings suggest that nuclear factor one regulates both proliferation and migration during the development of the subventricular zone neurogenic niche.
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 is a downstream target of NFIX during development of the forebrain.
The findings demonstrate that the level of Nfix expression during development and within the adult is essential for the function of the hippocampus during learning and memory.
Nfix is a novel regulator of murine hematopoietic stem and progenitor cell survival.
NFIX is robustly induced when neural stem cells enter quiescence
During vertebrate evolution, the transcription factor Nfix lost some specific functions, probably as a consequence of the different environment in which teleosts and mammals develop.
NFIX downregulation might independently predict poor prognosis in LUAD. DNA hypermethylation might be an important cause of the downregulation
Malan syndrome is caused by deletions or point mutations of NFIX clustered mostly in exon 2. There is no genotype-phenotype correlation except for an increased risk for epilepsy with 19p13.2 microdeletions. Variants arose de novo, except in one family in which mother was mosaic. Variants causing Malan and Marshall-Smith syndrome can be discerned by differences in the site of stop codon formation
It showing the contribution of NFIX to muscle development and muscular dystrophies, hematopoiesis, cancer, and neural stem cell biology, highlighting the importance of this knowledge in the development of therapeutic targets.
We identified recurrent targeting of NFIX by HPV16 insertion in anal carcinomas, supporting a role for this gene in oncogenesis
Microduplications encompassing NFIX cause intellectual disability, short stature and small head circumference.
Compared to noncancerous esophageal mucosa, miR-1290 expression was upregulated, while NFIX mRNA expression was downregulated in ESCC tissues. Data suggest that the dysregulation of miR-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.
Studies indicate the role of nuclear factor one (NFIs) as epigenetic regulators in cancer.
Plasma miR-1914* and -1915 interact with NFIX RNA.
Report novel mutations of NFIX gene causing Marshall-Smith syndrome or Sotos-like syndrome.
miR-1290 functions as a tumor oncogene 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-mediated suppression of ANT2 through NF1/Smad4 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 shows genome-wide association of NFIX, RAPGEF2 and MSRB3 with gestational age at birth.
NFI-X3 and STAT3 control the migration of differentiating astrocytes as well as migration and invasion of glioma cells via regulating YKL-40 expression.
NFI-X3 activates GFAP expression, in part, by inducing alterations in the nucleosome architecture that lead to the increased recruitment of RNA polymerase II
These findings demonstrate that allelic NFIX mutations trigger distinct phenotypes, depending specifically on their impact on nonsense-mediated mRNA decay.
Nuclear factor IA may play a role in astrocytoma biology.
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