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Microduplications encompassing NFIX cause intellectual disability, short stature and small head circumference.
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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.
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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.
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Studies indicate the role of nuclear factor one (NFIs) as epigenetic regulators in cancer.
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Plasma miR-1914* and -1915 interact with NFIX RNA.
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Report novel mutations of NFIX gene causing Marshall-Smith syndrome or Sotos-like syndrome.
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miR-1290 functions as a tumor oncogene in the progression of esophageal squamous cell carcinoma by targeting NFIX
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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.
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TGF-beta-mediated suppression of ANT2 through NF1/Smad4 complexes contributes to oxidative stress and DNA damage during induction of cellular senescence.
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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.
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missense mutations in NFIX were able to cause Sotos-like features.
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DNA methylation shows genome-wide association of NFIX, RAPGEF2 and MSRB3 with gestational age at birth.
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NFI-X3 and STAT3 control the migration of differentiating astrocytes as well as migration and invasion of glioma cells via regulating YKL-40 expression.
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NFI-X3 activates GFAP expression, in part, by inducing alterations in the nucleosome architecture that lead to the increased recruitment of RNA polymerase II
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These findings demonstrate that allelic NFIX mutations trigger distinct phenotypes, depending specifically on their impact on nonsense-mediated mRNA decay.
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Nuclear factor IA may play a role in astrocytoma biology.
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NFI-X cooperates with (activator protein 1)AP-1 by an unknown mechanism in astrocytes, which results in the expression of a subset of astrocyte-specific genes.
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temporal and dose-dependent interference by an AP-1 family member, c-Jun, upon NF-1 proteins binding an NF-1 consensus site derived from JC virus promoter sequence
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First report of structural alterations of the NFIA gene in hematopoietic diseases (polycythemia vera and chronic myelomonocytic leukemia, type 1).
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an expression program of NFIs is executed during the differentiation of astrocytes, with NFI-X and -C controlling the expression of astrocytic markers at late stages of differentiation.
