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AP1 transcription factors in epidermal differentiation and skin cancer.

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TLDR
It is suggested that individual AP1 transcription factors have different functions in the epidermis and in cancer development and that alteringAP1 transcription factor function in the basal versus suprabasal layers differentially influences theEpidermal differentiation response and disease and cancer development.
Abstract
AP1 (jun/fos) transcription factors (c-jun, junB, junD, c-fos, FosB, Fra-1, and Fra-2) are key regulators of epidermal keratinocyte survival and differentiation and important drivers of cancer development. Understanding the role of these factors in epidermis is complicated by the fact that each protein is expressed, at different levels, in multiple cells layers in differentiating epidermis, and because AP1 transcription factors regulate competing processes (i.e., proliferation, apoptosis, and differentiation). Various in vivo genetic approaches have been used to study these proteins including targeted and conditional knockdown, overexpression, and expression of dominant-negative inactivating AP1 transcription factors in epidermis. Taken together, these studies suggest that individual AP1 transcription factors have different functions in the epidermis and in cancer development and that altering AP1 transcription factor function in the basal versus suprabasal layers differentially influences the epidermal differentiation response and disease and cancer development.

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Journal ArticleDOI

Coupled Single-Cell CRISPR Screening and Epigenomic Profiling Reveals Causal Gene Regulatory Networks

TL;DR: Perturb-ATAC is a powerful strategy to dissect gene regulatory networks in development and disease based on the simultaneous detection of CRISPR guide RNAs and open chromatin sites by assay of transposase-accessible chromatin with sequencing (ATAC-seq).
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Deconstructing Olfactory Stem Cell Trajectories at Single-Cell Resolution

TL;DR: It is demonstrated that Wnt signaling regulates stem cell fate by promoting neuronal fate choices, and provides a model for deconstructing similar hierarchies in other stem cell niches.
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Hijacking of the AP-1 Signaling Pathway during Development of ATL.

TL;DR: The current thinking behind deregulation of the AP-1 pathway and its contribution to HTLV-induced cellular transformation is reviewed.
References
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Journal ArticleDOI

AP-1 function and regulation.

TL;DR: This work has shown that regulation by heterodimerization between Jun, Fos and ATF proteins, AP-1 activity is regulated through interactions with specific protein kinases and a variety of transcriptional coactivators, and there has been considerable progress in understanding some of the mechanisms and signaling pathways involved in the regulation of AP.
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AP-1 as a regulator of cell life and death

TL;DR: Interestingly, the growth-promoting activity of c-Jun is mediated by repression of tumour suppressors, as well as upregulation of positive cell cycle regulators, whereas JunB has the converse effect.
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Mitogen-activated protein kinase pathways.

TL;DR: Recent advances in the study of mitogen-activated protein kinase cascades include the cloning of genes encoding novel members of the cascades, further definition of the roles of the cascade in responses to extracellular signals, and examination of cross-talk between different cascades.
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The Regulation of AP-1 Activity by Mitogen-activated Protein Kinases

TL;DR: The specific roles of three MAPKs, namely ERK, JNK and FRK, in modulation of both the level and activity of AP-1, are discussed.
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AP-1: a double-edged sword in tumorigenesis

TL;DR: This work focuses on the JUN and FOS proteins and aims to offer a new perspective on the molecular mechanisms that regulate the oncogenic and anti-oncogenic effects of AP-1 in tumour development.
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