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Anti-NFIB antibody produced in rabbit

RRID:AB_1854424

Antibody ID

AB_1854424

Target Antigen

NFIB antibody produced in rabbit human, human

Proper Citation

(Sigma-Aldrich Cat# HPA003956, RRID:AB_1854424)

Clonality

polyclonal antibody

Comments

Vendor recommendations: indirect immunofluorescence: suitable, immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable, protein array: suitable, immunoblotting: suitable; Immunofluorescence; Immunohistochemistry; Other; Western Blot

Host Organism

rabbit

Vendor

Sigma-Aldrich

Cat Num

HPA003956

Publications that use this research resource

Differential neuronal and glial expression of nuclear factor I proteins in the cerebral cortex of adult mice.

  • Chen KS
  • J. Comp. Neurol.
  • 2017 Aug 1

Literature context:


Abstract:

The nuclear factor I (NFI) family of transcription factors plays an important role in the development of the cerebral cortex in humans and mice. Disruption of nuclear factor IA (NFIA), nuclear factor IB (NFIB), or nuclear factor IX (NFIX) results in abnormal development of the corpus callosum, lateral ventricles, and hippocampus. However, the expression or function of these genes has not been examined in detail in the adult brain, and the cell type-specific expression of NFIA, NFIB, and NFIX is currently unknown. Here, we demonstrate that the expression of each NFI protein shows a distinct laminar pattern in the adult mouse neocortex and that their cell type-specific expression differs depending on the family member. NFIA expression was more frequently observed in astrocytes and oligodendroglia, whereas NFIB expression was predominantly localized to astrocytes and neurons. NFIX expression was most commonly observed in neurons. The NFI proteins were equally distributed within microglia, and the ependymal cells lining the ventricles of the brain expressed all three proteins. In the hippocampus, the NFI proteins were expressed during all stages of neural stem cell differentiation in the dentate gyrus, with higher expression intensity in neuroblast cells as compared to quiescent stem cells and mature granule neurons. These findings suggest that the NFI proteins may play distinct roles in cell lineage specification or maintenance, and establish the basis for further investigation of their function in the adult brain and their emerging role in disease.

Nfib Regulates Transcriptional Networks That Control the Development of Prostatic Hyperplasia.

  • Grabowska MM
  • Endocrinology
  • 2016 Mar 27

Literature context:


Abstract:

A functional complex consisting of androgen receptor (AR) and forkhead box A1 (FOXA1) proteins supports prostatic development, differentiation, and disease. In addition, the interaction of FOXA1 with cofactors such as nuclear factor I (NFI) family members modulates AR target gene expression. However, the global role of specific NFI family members has yet to be described in the prostate. In these studies, chromatin immunoprecipitation followed by DNA sequencing in androgen-dependent LNCaP prostate cancer cells demonstrated that 64.3% of NFIB binding sites are associated with AR and FOXA1 binding sites. Interrogation of published data revealed that genes associated with NFIB binding sites are predominantly induced after dihydrotestosterone treatment of LNCaP cells, whereas NFIB knockdown studies demonstrated that loss of NFIB drives increased AR expression and superinduction of a subset of AR target genes. Notably, genes bound by NFIB only are associated with cell division and cell cycle. To define the role of NFIB in vivo, mouse Nfib knockout prostatic tissue was rescued via renal capsule engraftment. Loss of Nfib expression resulted in prostatic hyperplasia, which did not resolve in response to castration, and an expansion of an intermediate cell population in a small subset of grafts. In human benign prostatic hyperplasia, luminal NFIB loss correlated with more severe disease. Finally, some areas of intermediate cell expansion were also associated with NFIB loss. Taken together, these results show a fundamental role for NFIB as a coregulator of AR action in the prostate and in controlling prostatic hyperplasia.

Funding information:
  • NINDS NIH HHS - R01 NS083898(United States)