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IKKα signaling in the nucleus or cytoplasm of keratinocytes leads to opposite skin phenotypes.

ABSTRACT: IKKα signaling in the nucleus or cytoplasm of keratinocytes leads to opposite skin phenotypes.

PROVIDER: PRJNA999660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25448780_1.fastq.gz	Fastqsanger.gz
	SRR25448780_2.fastq.gz	Fastqsanger.gz
	SRR25448781_1.fastq.gz	Fastqsanger.gz
	SRR25448781_2.fastq.gz	Fastqsanger.gz
	SRR25448782_1.fastq.gz	Fastqsanger.gz

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IKKα signaling in the nucleus or cytoplasm of keratinocytes leads to opposite skin phenotypes.

Project description:The skin exerts essential roles for the organism survival, such as environmental barrier and immune functions. IKKα is known as an essential protein for skin homeostasis. However, the functions performed by IKKα in the skin and the mechanisms it employs are largely unknown, leading to contradictory interpretations and results regarding the consequences of its deregulation in pathologies such as non-melanoma skin cancer (NMSC). Here, using our previously generated transgenic mouse models which express IKKα in the cytoplasm (C-IKKα mice) or in the nucleus (N-IKKα mice) of basal keratinocytes, we demonstrate that at each subcellular localization, IKKα distinctly regulates signaling pathways important for maintaining the balance between keratinocyte proliferation and differentiation, as well as the inflammatory response of the skin. As a result, N-IKKα mice show an atrophic epidermis with exacerbated terminal differentiation, reminiscent of alterations observed in patients with ichthyosis. Conversely, C-IKKα mice display a hyperplastic epidermis with impaired epidermal differentiation and pustular inflammation, resembling patients with pustular psoriasis. Interestingly, C-IKKα keratinocytes are almost devoid of nuclear IKKα due to endogenous IKKα downregulation. However, these changes in the skin of C-IKKα mice do not lead to the development of squamous cell carcinomas (SCCs), unlike N-IKKα mice, which develop spontaneous SCCs.

2024-11-14 | GSE239533 | GEO

FMRP deficiency leads to multifactorial dysregulation of splicing and mislocalization of MBNL1 to the cytoplasm

Project description:FMRP deficiency leads to multifactorial dysregulation of splicing and mislocalization of MBNL1 to the cytoplasm

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IKKα Is Required to Maintain Skin Homeostasis and Prevent Skin Cancer

Project description:It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear, however, whether there are any innate surveillants that ensure keratinocytes undergoing terminal differentiation, preventing the disease. IKKα induces keratinocyte terminal differentiation and its reduction promotes skin tumor development. However, its nature function in skin cancer is unknown. Here we found that mice with IKKα deletion in keratinocytes or in hair follicle keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKα inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through an EGFR-driven autocrine loop in mice. Thus, IKKα serves as an innate surveillant.

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Compression Xylem vs. Opposite Xylem

Project description:Compression Xylem vs. Opposite Xylem

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Regulation of epidermal differentiation through KDF1-mediated deubiquitination of IKKα

Project description:Progenitor cells at the basal layer of skin epidermis play an essential role in maintaining tissue homeostasis and enhancing wound repair in skin. The proliferation, differentiation, and cell death of epidermal progenitor cells have to be delicately regulated, as deregulation of this process can lead to many skin diseases, including skin cancers. However, the underlying molecular mechanisms involved in skin homeostasis remain poorly defined. In this study, with quantitative proteomics approach, we identified an important interaction between KDF1 (Keratinocyte Differentiation Factor 1) and IKKα (IκB kinase α) in differentiating skin keratinocytes. Ablation of either KDF1 or IKKα in mice leads to similar but striking abnormalities in skin development, particularly in skin epidermal differentiation. With biochemical and mouse genetics approach, we further demonstrate that the interaction of IKKα and KDF1 is essential for epidermal differentiation. To probe deeper into the mechanisms, we find that KDF1 associates with a deubiquitinating protease, USP7 (Ubiquitin Specific Peptidase 7), and KDF1 can regulate skin differentiation through deubiquitination and stabilization of IKKα. Taken together, our study unravels an important molecular mechanism underlying skin tissue homeostasis and epidermal differentiation.

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DNA Repair Inhibition Leads to Active Export of Repetitive Sequences to the Cytoplasm Triggering an Inflammatory Response

Project description:DNA Repair Inhibition Leads to Active Export of Repetitive Sequences to the Cytoplasm Triggering an Inflammatory Response

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Dioscorea opposite

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Compression Xylem vs. Opposite Xylem

Project description:This SuperSeries is composed of the following subset Series: GSE37678: cDNA Microarray 1: Compression Xylem vs. Opposite Xylem GSE37736: cDNA Microarray 2: Compression Xylem vs. Opposite Xylem Refer to individual Series

2012-05-05 | E-GEOD-37789 | biostudies-arrayexpress

ITGA3 neg. human keratinocytes

Project description:Integrin alpha3beta1, a major epidermal adhesion receptor is critical for organization of the basement membrane during development and wound healing. Integrin alpha3 deficiency leads to interstitial lung disease, nephrotic syndrome and epidermolysis bullosa (ILNEB), an autosomal recessive multiorgan disease characterized by basement membrane abnormalities in skin, lung and kidney. The pathogenetic chains from ITGA3 mutation to tissue abnormalities are still unclear. Although integrin 3 was reported to regulate multiple extracellular proteins, the composition of the extracellular compartment of integrin alpha3-negative keratinocytes has not been resolved so far. In a comprehensive approach, quantitative proteomics of deposited extracellular matrix, conditioned cultured media as well as of the intracellular compartment of keratinocytes isolated from an ILNEB patient and from normal skin were performed. By mass spectrometry-based proteomics, 167 proteins corresponding to the GO terms “extracellular” and “cell adhesion”, or included in the “human matrisome” were identified in the deposited extracellular matrix, and 217 in the conditioned media of normal human keratinocytes. In the absence of integrin alpha3, 33% and 26% respectively were dysregulated. Dysregulated proteins were functionally related to integrin alpha3 or were known interaction partners. The results show that in the absence of integrin alpha3 ILNEB keratinocytes produce a fibronectin-rich microenvironment and make use of fibronectin-binding integrin subunits alphav and alpha5.

2018-11-27 | PXD009896 | Pride

Genome-wide maps of Gata6 in primary mouse keratinocytes

Project description:In adult K14Î?NLef1 mouse, the overexpression of â??NLef1, a Ã?-catenin dominat negative, in basal keratinocytes leads to the conversion of hair follicles into multilayered epithelial cysts and ectopic sebaceous gland. â??NLef1 transcriptional activity led to Gata6 overexpression in the pilosebaceous unit in transgenic mice. To uncover direct target genes of Gata6 we performed ChIP-Seq experiments in primary mouse keratinocytes. Examination of Gata6 genomic targets in mouse primary keratinocytes

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