anti-Nuclear Factor I/A (NFIA) Antibodies

Human Nuclear Factor I/A (NFIA) interaction partners

1. This study reveals NFIA as a pro-endocrine factor in the pancreas, acting to repress Mib1, inhibit Dll1 endocytosis and thus promote escape from Notch activation.

2. High Nuclear factor I A expresion is associated with temozolomide resistance in glioblastoma via activation of nuclear factor kappaB pathway.

3. High NFIA expression in tumors of patients with esophageal squamous cell carcinoma (ESCC) is correlated with lymph node metastasis and poor differentiation. NFIA is found to be an independent predictor of poor prognosis in patients with ESCC.

4. Transient expression of NFIA is sufficient to trigger glial competency of human pluripotent stem cell-derived neural stem cells within 5 days and to convert these cells into astrocytes in the presence of glial-promoting factors, as compared to 3-6 months using current protocols.

5. The consistent overlap in clinical presentation provides further evidence of the critical role of NFIA haploinsufficiency in the development of the 1p32-p31 microdeletion syndrome phenotype.

6. Data define a previously unknown nuclear factor I-A-nuclear factor-kappaB feed-forward regulation that may contribute to glioblastoma cell survival.

7. Studies indicate the role of nuclear factor one (NFIs) as epigenetic regulators in cancer.

8. Altogether, these results demonstrated that miR-370 suppressed hepatitis B virus gene expression and replication through repressing NFIA expression, which stimulates hepatitis B virus replication via direct regulation on hepatitis B virus Enhancer I activities.

9. We verified that NFIA binds to the IGFBP2 promoter and transcriptionally enhances IGFBP2 expression levels. We identified that NFIA-mediated IGFBP2 signaling pathways are involved in miR-302b-induced glioma cell death.

10. miR-191 was upregulated in patients with middle- and late-stage NSCLC, and in NSCLC cell lines, under mild hypoxic conditions. miR-191 promoted the proliferation and migration of NSCLC under chronic hypoxic conditions, and this promotion may be associated with its targeting of NFIA.

11. Dihydrocapsaicin can significantly decrease proinflammatory cytokines through enhancing NFIA and inhibiting NF-kappaB expression

12. These results demonstrated that RP5833A20.1 inhibited tumor cell proliferation, induced apoptosis and inhibited cellcycle progression by suppressing the expression of NFIA in U251 cells.

13. NFI-A is involved in the miR-21-induced expression of IL-10 in B cells in nasopharyngeal carcinoma; Il-10 is capable of suppressing CD8+ T-cell activities.

14. microRNA-136 targeted and degraded NFIA, which induced the release of microRNA-223, promoting CD11b expression. Direct base pairing occurs between miR-136 and the 3' UTR of NFIA mRNA.

15. this family also carried a microdeletion affecting solely the NFIA gene, this study substantiates the importance of this gene in craniofacial development.

16. TGF-beta-mediated suppression of ANT2 through NF1/Smad4 complexes contributes to oxidative stress and DNA damage during induction of cellular senescence.

17. a strong candidate gene for asthma and allergic rhinitis

18. RP5-833A20.1/miR-382-5p/NFIA pathway was essential to the regulation of cholesterol homeostasis and inflammatory reactions.

19. This report presents the first case of an intragenic deletion within the NFIA gene that is still consistent with classic clinical phenotypes present in previously reported cases of chromosome 1p31.3 related deletion.

20. High nuclear factor IA expression is associated with glioblastomas.

Mouse (Murine) Nuclear Factor I/A (NFIA) interaction partners

1. This study reveals NFIA as a pro-endocrine factor in the pancreas, acting to repress Mib1, inhibit Dll1 endocytosis and thus promote escape from Notch activation.

2. It identified NFIA and ATF3 as drivers of astrocyte differentiation from neural precursor cells while RUNX2 promotes astrocyte maturation.

3. Our results support a myeloid cell loop in which NFI-A and miR-21 and miR-181b sustain Gr1(+)CD11b(+) MDSC-dependent immunosuppression during

4. Of these, NFIA emerged as the regulator yielding the strongest molecular and cellular phenotypes. To examine its regulatory function, we profiled the genomic localization of NFIA, identifying it as a key early regulator of terminal brown fat cell differentiation.

5. PAX6 can substitute for LHX2 and override NFIA-induced astrogliogenesis in developing hippocampus in vivo.

6. The NFIA identifies a subset of bipolar cells as well as Muller glia and astrocytes. During early postnatal development, NFIA labels astrocytes on the day of birth, AII amacrine cells at postnatal (P) day 5, and Muller glia by P10, when horizontal cells also transiently exhibit NFIA immunofluorescence.

7. NFIA expression regulates glioma tumorigenesis and glia-specific enhancers enhancers contribute to glioma formation.

8. NFIA activates the cell-type-specific enhancers and facilitates the binding of PPARgamma to control the brown fat gene program.

9. Dihydrocapsaicin can significantly decrease proinflammatory cytokines through enhancing NFIA and inhibiting NF-kappaB expression

10. Astrocyte induction by Zbtb20 is suppressed by knockdown of NFIA.

11. NFI-A disrupts myeloid cell differentiation and maturation in septic mice

12. NFIA and NFIB are endogenously expressed in gradients with high caudo-medial to low rostro-lateral expression ... this expression pattern deviates from that of PAX6, suggesting that PAX6 does not drive Nfi expression

13. RP5-833A20.1/miR-382-5p/NFIA pathway was essential to the regulation of cholesterol homeostasis and inflammatory reactions.

14. Nfia cooperates with sonic hedgehog signaling to initiate medulloblastoma.

15. Our data thus suggest that NFI nucleosomal interaction may contribute to the partitioning of distinct chromatin domains and to epigenetic gene expression regulation

16. As maturing cerebellar granule neurons become more hyperpolarized, NFATc4 binding declines leading to onset of NFI temporal binding and the NFI switch program

17. NFIA and NFIB are expressed in both the developing and the adult olfactory bulb indicative of a regulatory role for these transcription factors in the development of this facet of the olfactory system.

18. NFIA is expressed in oligodendrocyte progenitors, but not differentiated oligodendrocytes during mouse embryonic development.

19. NFIA is a transcription factor that plays a crucial role in the onset of gliogenesis; we found that its induction is regulated by the transcription factor Sox9 and that this relationship mediates the initiation of gliogenesis

20. The studies demonstrate for the first time a requirement for the NFI-A transcription factor in antigen receptor-induced T-cell activation events.