anti-Nuclear Factor I/C (CCAAT-Binding Transcription Factor) (NFIC) Antibodies

Mouse (Murine) Nuclear Factor I/C (CCAAT-Binding Transcription Factor) (NFIC) interaction partners

1. the Runx2-Nfic-Osx pathway is one of the key factors that regulate ameloblast differentiation.

2. An Nfic-Hhip-Hh signaling pathway is crucial for apical papilla growth and proper root formation.

3. NFI-C acts as a regulator of the phased hepatocyte proliferation during liver regeneration.

4. Results suggest that NFI-C acts as a transcriptional switch in cell fate determination between osteoblast and adipocyte differentiation in BMSCs.

5. The purpose of this study was to identify the molecular interactions between NFI-C and TGF-beta1 signaling in mouse odontoblasts.

6. The data suggest that zinc equilibrium is required for odontoblast differentiation and dentin formation during dentinogenesis through the nuclear accumulation and modulation of NFI-C.

7. Nuclear factor I-C regulates TGF-{beta}-dependent hair follicle cycling

8. elongation of dental epithelial cells, HERS, is essential for root development and that TGF-beta/BMP signaling relies on a Smad4-dependent signaling mechanism to regulate Nfic expression via Shh signaling to control root formation.

9. Nfic(-/-) mice have unique tooth pathologies: molars lacking roots, thin and brittle mandibular incisors, and weakened abnormal maxillary incisors.

10. first report demostrating the importance of NF1 proteins in the p53 gene activation in the mouse mammary gland; also, first time that p53 gene activation shown to be coupled to a specific, endogenously expressed NF1 isoform

11. NF1-C2 protein is present in the epithelial compartment at the virgin stage and throughout mammary gland development and its transcripts are expressed in the whole epithelium at pregnancy as well as the lactation stage.

12. Data demonstrate that nuclear Jak2 regulates the amount of active NF1-C2 through tyrosine phosphorylation and proteasomal degradation.

13. the chromatin architecture of the promoters does not permit strong association of GR in the absence of NF1

14. may be a key regulator of root odontoblast differentiation and root formation

15. Loss of the Nfic gene interferes with the formation of intercellular junctions that causes aberrant odontoblast differentiation and abnormal dentin formation.

16. loss of Nfic leads to the suppression of odontogenic cell proliferation and differentiation and induces apoptosis of aberrant odontoblasts during root formation, thereby contributing to the formation of short roots

Human Nuclear Factor I/C (CCAAT-Binding Transcription Factor) (NFIC) interaction partners

1. Genome-wide significant (GWS) associations in single-nucleotide polymorphism (SNP)-based tests (P < 5 x 10(-8)) were identified for the interaction of the (apolipoprotein E) APOE epsilon4 allele with NFIC SNP.

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

3. Nuclear factor I-C regulates E-cadherin via control of KLF4 in breast cancer

4. Results suggest that NFI-C acts as a transcriptional switch in cell fate determination between osteoblast and adipocyte differentiation in BMSCs.

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

6. Over-expression of NFIC increased cell proliferation, mineralization nodule formation and alkaline phosphatase activity in stem cells from the apical papilla.

7. transcription factor Nuclear Factor 1-C (NF1C) as a candidate to regulate AHR transcription in a polymorphism-dependent manner

8. These data suggest a critical role for calcineurin in NFI transcriptional regulation and in the determination of malignant glioma infiltrative properties.

9. the influence of i3T3 on the expression and DNA binding of NFI, another TF important for cell proliferation and cell cycle progression

10. novel role of NF1-C2 in tumor development and epithelial-to-mesenchymal transition in breast cancer; NF1-C2 is lost during tumor progression and virtully absent from lymph node metastases; FoxF1 was was found to be a direct repressed target of NF1-C2

11. A specific region (-688 to -611 bp) was discovered in the IRS2 promoter essential for basal promoter activity and oxidative stress induced transcription depending on ERK activation and SP1 and NFI binding in human hepatocytes.

12. diminished NF-1C-dependent repression may be one mechanism underlying increased basal CYP17 promoter activity and altered gene expression in PCOS (polycystic ovary syndrome) theca cells.

13. The BAF complex & NF1/CTF might act as components of the RNAP II holoenzyme to participate in formation of transcriptional pre-initiation complex.

14. Data demonstrate that nuclear Jak2 regulates the amount of active NF1-C2 through tyrosine phosphorylation and proteasomal degradation.

15. the chromatin architecture of the promoters does not permit strong association of GR in the absence of NF1

16. we suggest that bHLH factors recruit NFI to enhance skeletal muscle Na(+) channel expression.

17. All NFI isoforms were found to be expressed in human corneal epithelial cells grown on laminin.

18. These are the first studies to analyze the expression of NFI-C isoforms in dental versus nondental cells/tissues.

19. These results suggest that alpha5 gene expression is likely dictated by subtle alterations in the nuclear ratio of TFs that either repress (NFI) or activate (Sp1 and AP-1) alpha5 transcription in corneal epithelial cells.

20. Knockdown of NFIB and NFIC expression using siRNA decreased and increased IGFBP5 expression, respectively.