scholarly journals Expression and role of microRNA-212/nuclear factor I-A in depressive mice

Bioengineered ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 11520-11532
Author(s):  
Liang Si ◽  
Yanyan Wang ◽  
Min Liu ◽  
Lifeng Yang ◽  
Li Zhang
Keyword(s):  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I

scholarly journals Organization of the α-Globin Promoter and Possible Role of Nuclear Factor I in an α-Globin-inducible and in a Noninducible Cell Line

1995 ◽  
Vol 270 (33) ◽  
pp. 19643-19650 ◽  
Author(s):  
Theo Rein ◽  
Reinhold Förster ◽  
Anja Krause ◽  
Ernst-L. Winnacker ◽  
Haralabos Zorbas
Keyword(s):  
Cell Line ◽  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I ◽  
Globin Promoter

scholarly journals Nuclear Factor I-C Links Platelet-Derived Growth Factor and Transforming Growth Factor β1 Signaling to Skin Wound Healing Progression

2009 ◽  
Vol 29 (22) ◽  
pp. 6006-6017 ◽  
Author(s):  
Genta Plasari ◽  
Alessandra Calabrese ◽  
Yves Dusserre ◽  
Richard M. Gronostajski ◽  
Alan Mcnair ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Wound Closure ◽  
Transforming Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Nuclear Factor ◽  
Matrix Deposition ◽  
Factor I ◽  
Nuclear Factor I

ABSTRACT Transforming growth factor β (TGF-β) and platelet-derived growth factor A (PDGFΑ) play a central role in tissue morphogenesis and repair, but their interplay remain poorly understood. The nuclear factor I C (NFI-C) transcription factor has been implicated in TGF-β signaling, extracellular matrix deposition, and skin appendage pathologies, but a potential role in skin morphogenesis or healing had not been assessed. To evaluate this possibility, we performed a global gene expression analysis in NFI-C−/− and wild-type embryonic primary murine fibroblasts. This indicated that NFI-C acts mostly to repress gene expression in response to TGF-β1. Misregulated genes were prominently overrepresented by regulators of connective tissue inflammation and repair. In vivo skin healing revealed a faster inflammatory stage and wound closure in NFI-C−/− mice. Expression of PDGFA and PDGF-receptor alpha were increased in wounds of NFI-C−/− mice, explaining the early recruitment of macrophages and fibroblasts. Differentiation of fibroblasts to contractile myofibroblasts was also elevated, providing a rationale for faster wound closure. Taken together with the role of TGF-β in myofibroblast differentiation, our results imply a central role of NFI-C in the interplay of the two signaling pathways and in regulation of the progression of tissue regeneration.

The Critical Role of Nuclear Factor I‐C in Tooth Development

Oral Diseases ◽  
2021 ◽  
Author(s):  
Chunmei Xu ◽  
Xudong Xie ◽  
Lei Zhao ◽  
Yafei Wu ◽  
Jun Wang
Keyword(s):  
Tooth Development ◽  
Critical Role ◽  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I

scholarly journals Nuclear factor I-C disrupts cellular homeostasis between autophagy and apoptosis via miR-200b-Ambra1 in neural tube defects

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wanqi Huang ◽  
Tianchu Huang ◽  
Yusi Liu ◽  
Jialin Fu ◽  
Xiaowei Wei ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Critical Role ◽  
Neural Tube Closure ◽  
Nuclear Factor ◽  
Cellular Homeostasis ◽  
Factor I ◽  
Nuclear Factor I ◽  
Insight Into

AbstractImpaired autophagy and excessive apoptosis disrupt cellular homeostasis and contribute to neural tube defects (NTDs), which are a group of fatal and disabling birth defects caused by the failure of neural tube closure during early embryonic development. However, the regulatory mechanisms underlying NTDs and outcomes remain elusive. Here, we report the role of the transcription factor nuclear factor I-C (NFIC) in maintaining cellular homeostasis in NTDs. We demonstrated that abnormally elevated levels of NFIC in a mouse model of NTDs can interact with the miR-200b promoter, leading to the activation of the transcription of miR-200b, which plays a critical role in NTD formation, as reported in our previous study. Furthermore, miR-200b represses autophagy and triggers apoptosis by directly targeting the autophagy-related gene Ambra1 (Autophagy/Beclin1 regulator 1). Notably, miR-200b inhibitors mitigate the unexpected effects of NFIC on autophagy and apoptosis. Collectively, these results indicate that the NFIC-miR-200b-Ambra1 axis, which integrates transcription- and epigenome-regulated miRNAs and an autophagy regulator, disrupts cellular homeostasis during the closure of the neural tube, and may provide new insight into NTD pathogenesis.

scholarly journals The repression of nuclear factor I/CCAAT transcription factor (NFI/CTF) transactivating domain by oxidative stress is mediated by a critical cysteine (Cys-427)

2000 ◽  
Vol 348 (1) ◽  
pp. 235-240 ◽  
Author(s):  
Yannick MOREL ◽  
Robert BAROUKI
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Critical Role ◽  
Point Mutations ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I

The activity of the nuclear factor I/CCAAT transcription factor (NFI/CTF) is negatively regulated by oxidative stress. The addition of relatively high (millimolar) H2O2 concentrations inactivates cellular NFI DNA-binding activity whereas lower concentrations can repress NFI/CTF transactivating function. We have investigated the mechanism of this regulation using Gal4 fusion proteins and transfection assays. We show that micromolar H2O2 concentrations repress the transactivating domain of NFI/CTF in a dose-dependent manner and are less or not active on other transcription factors' transactivating domains. Studies using deletions and point mutations pointed to the critical role of Cys-427. Indeed, when this cysteine is mutated into a serine, the repression by H2O2 is totally blunted. Mutation of other cysteine, serine and tyrosine residues within the transactivating domain had no clear effect on the repression by H2O2. Finally, treatment of cells with the thiol-alkylating reagent N-ethylmaleimide leads to a decrease in the transactivating function, which is dependent on Cys-427. This study shows that transactivating domains of transcription factors can constitute very sensitive targets of oxidative stress and highlights the critical role of these domains.

Studies of nuclear factor I/X (NFIX) mutations causing the Marshall-Smith syndrome (MSS)

2017 ◽  
Author(s):  
Kreepa Kooblall ◽  
Mark Stevenson ◽  
Raoul Hennekam ◽  
Rajesh Thakker
Keyword(s):  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I
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