Dataset Information

KDF1 interacting protein in the ameloblast cell line

ABSTRACT: Keratinocyte differentiation factor 1 (KDF1) was recently identified as a rare candidate gene of human congenital tooth agenesis. Extensive studies using mouse models have revealed the role of KDF1 in the development of epithelium-derived organs. For example, a study reported that KDF1 mutant mice Kdf1GT/GT exhibited enhanced proliferation and restricted differentiation of epidermal keratinocytes. Furthermore, preliminary findings reported that Kdf1 was mainly expressed in the inner enamel epithelium, which is the pre-differentiated form of ameloblasts, a dental epithelial cell, during tooth development. Thus, we hypothesized that KDF1 plays a crucial role in the differentiation of ameloblast and conducted in vitro experiments to investigate the role of KDF1 in ameloblast differentiation. As the robust evidence to clarify the mechanism through which KDF1 regulates ameloblast differentiation, LS-MS was employed to identify the possible proteins that can interact with KDF1. Thus, the raw data of LS-MS of this project are deposited in iProX database for further investigations. This study is the first to reveal the KDF1-mediated protein interaction network in ameloblast differentiation, not only providing help to broaden the functional cognition of KDF1, but also contributing to enhance the understanding of the gene regulatory network of enamel development.

ORGANISM(S): Mus Musculus

SUBMITTER: Dong Han

PROVIDER: PXD048592 | iProX | Tue Jan 16 00:00:00 GMT 2024

REPOSITORIES: iProX

ACCESS DATA

Similar Datasets

Project description:M cells in the follicle-associated epithelium (FAE) of Peyer’s patches (PPs) serve as a main portal for external antigens. Limitation in the number of M cells has hampered identification of their specific molecules until recently. Efforts by us as well as others has gradually unraveled the molecular mechanisms for the development and differentiation of M cells. However, molecular mechanisms of antigen transcytosis and M cell differentiation were not fully elucidated. Recent studies reported that small non-coding RNAs including microRNA (miRNA) regulate gene expression that controls various biological processes such as cellular differentiation and functions. In fact, intestinal epithelial miRNAs play a critical role in goblet cell differentiation and maturation. However, the expression and function of miRNAs in FAE including M cell that function as the sentinels in the mucosal immune system are largely unknown. To address this notion, we performed microarray analysis to characterize expression profiles of miRNA in intestinal villous epithelium (VE) and FAE of PP. We also generated mice with intestinal epithelial cell-specific deletion of Dicer1 (DicerΔIEC), in which intestinal phenotypes including M-cell differentiation and epithelial morphology were examined. The microarray analysis identified that 72 miRNAs were up-regulated whereas 11 miRNAs were down-regulated, in FAE compared to VE. DicerΔIEC mice displayed a prominent decrease in mature M cells, suggesting an essential role of miRNAs in maturation of the cell type. Furthermore, electron micrographs clearly showed that depletion of miRNA caused the loss of endosomal structures in M cells. In addition, antigen uptake in M cells was impaired in DicerΔIEC mice compared to control floxed Dicer mice. These results raised the possibility that miRNAs play a significant role in the regulation of M cells maturation, and consequently secure mucosal immune homeostasis. Follicle associated epithelium or villous epithelium was isolated from Peyer's patch(PP). PP was soaked Hank's balanced salt solution (HBSS;GIBCO) containing 30mM EDTA. After incubation at 4℃ for 20 min, FAE or VE was isolated by manipulation with fine needle under stereomicroscopic monitoring. The isolated epithelial cell sheets were kept in ice-cold HBSS until RNA extraction(n=2).

Dataset Information

KDF1 interacting protein in the ameloblast cell line

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets