High impact information on Nfic

• The Nfic mutation is the first mutation described that affects primarily tooth root formation and should greatly aid our understanding of postnatal tooth development [1].
• Heterozygous animals appear normal, whereas Nfic(-/-) mice have unique tooth pathologies: molars lacking roots, thin and brittle mandibular incisors, and weakened abnormal maxillary incisors [1].
• Although Nfic is expressed in many organ systems, including the developing tooth, the tooth root development defects were the prominent phenotype [1].
• The Psen1 C-terminal proteolytic fragment (CTF) is present at varying levels during embryogenesis, indicating the existence of developmental control mechanisms regulating its production [2].
• APP C-terminal fragments (CTF) were markedly increased in both endoplasmic reticulum- (ER-) and Golgi-rich fractions of fibroblasts from KO mice; moreover, similar increases were documented directly in KO brain tissue [3].

Biological context of Nfic

• It is most likely that this lactation/involution switch in NF1 factors represents a change in expression of NF1 C (CTF/NF1) proteins [4].
• We further demonstrate that purified NFI-C protein will bind to this positive regulatory region within the hSMUG1 gene [5].

Anatomical context of Nfic

• Overexpression of NFI-C in NIH-3T3 cells results in an increase in SMUG1 enzyme activity [5].

Associations of Nfic with chemical compounds

• Erythromycin and azithromycin were macrolide antibiotics that markedly changed the cleavage of the APP C-Terminal Fragment (CTF) in SH-SY5Y cells [6].

References