The GEF Bcr activates RhoA/MAL signaling to promote keratinocyte differentiation via desmoglein-1

Dubash, Adi D.; Koetsier, Jennifer L.; Amargo, Evangeline V.; Najor, Nicole A.; Harmon, Robert M.; Green, Kathleen J.

doi:10.1083/jcb.201304133

Cited by 37 publications

(27 citation statements)

References 75 publications

(107 reference statements)

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“…In addition, the receptor tyrosine kinase EphA2, in a ligand-dependent manner, promotes entry of keratinocytes into a terminal differentiation pathway through a mechanism reliant on Dsg1 (Lin et al 2010). Finally, the RhoA GEF breakpoint cluster region (Bcr) has been shown to promote keratinocyte differentiation through the regulation of MAL/SRF signaling, again in a manner that is dependent on Dsg1 (Dubash et al 2013). …”

Section: Desmosomal Cadherinsmentioning

confidence: 99%

Desmosome regulation and signaling in disease

2015

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Desmosomes are cell-cell adhesive organelles with a well-known role in forming strong intercellular adhesion during embryogenesis and in adult tissues subject to mechanical stress, such as the heart and skin. More recently, desmosome components have also emerged as cell signaling regulators. Loss of expression or interference with the function of desmosome molecules results in diseases of the heart and skin and contributes to cancer progression. However, the underlying molecular mechanisms that result in inherited and acquired disorders remain poorly understood. To address this question, researchers are directing their studies towards determining the functions that occur inside and outside of the junctions and the extent to which functions are adhesion-dependent or independent. This review focuses on recent discoveries that provide insights into the role of desmosomes and desmosome components in cell signaling and disease; wherever possible, we address molecular functions within and outside of the adhesive structure.

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Section: Desmosomal Cadherinsmentioning

confidence: 99%

Desmosome regulation and signaling in disease

2015

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“…Suppression of PKC-a or PKC-d isoforms increases Dsg3 expression, whereas suppression of PKC-d and PKC-1 isoforms either decreases or increases Dsg1 levels, respectively (Szegedi et al 2009 (Roemer 2012) and p63 has been shown by chromatin immunoprecipitation (ChIP) to bind and activate Dsg1, Dsc3, and Dp promoters (Ferone et al 2013;Johnson et al 2014). Rho-mediated changes in the actin cytoskeleton lead to changes in Srf-dependent transcription (Miralles et al 2003) and Srf controls the expression of Pkp2 and Dsg1, which in turn drives a program of terminal differentiation (Leitner et al 2011;Dubash et al 2013), The Wnt-regulated TCF/Lef transcription complex has been implicated in regulation of Dsg4, Dsc2, Dsc3, and Pg expression but direct binding of these transcription factors to desmosomal component promoters has only been shown in a few instances (Table 1) (Bazzi et al 2009;Bailey et al 2012;Tokonzaba et al 2013). Pg itself complexes with TCF/ Lef-1 to regulate the balance of Dsc2 and Dsc3 expression (Tokonzaba et al 2013).…”

Section: Transcriptional Regulation Of Desmosomal Componentsmentioning

confidence: 99%

Desmosomes: Regulators of Cellular Signaling and Adhesion in Epidermal Health and Disease

Johnson

Najor

Green

2014

Cold Spring Harbor Perspectives in Medicine

119

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“…DSG1 is a transmembrane glycoprotein. It is involved in regulating keratinocyte differentiation , epidermal differentiation and morphogenesis .…”

Section: Resultsmentioning

confidence: 99%

Effect of purified fractions from cell culture supernate of high‐density pre‐B acute lymphoblastic leukemia cells (ALL3) on the growth of ALL3 cells at low density

2016

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The mechanisms underlying the aberrant growth and interactions between cells are not understood very well. The pre-B acute lymphoblastic leukemia cells directly obtained from an adult patient grow very poorly or don't grow at all at low density (LD), but grow better at high starting cell density (HD). We found that the LD ALL3 cells can be stimulated to grow in the presence of diffusible, soluble factors secreted by ALL3 cells themselves growing at high starting cell density. We then developed a biochemical purification procedure that allowed us to purify the factor(s) with stimulatory activity and analyzed them by nanoliquid chromatography-tandem mass spectrometry (nanoLC-MS/MS). Using nanoLC-MS/MS we have identified several proteins which were further processed using various bioinformatics tools. This resulted in 8 protein candidates which might be responsible for the growth activity on non-growing LD ALL3 cells and their involvement in the stimulatory activity are discussed.

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The GEF Bcr activates RhoA/MAL signaling to promote keratinocyte differentiation via desmoglein-1

Abstract: The GEF Bcr promotes RhoA-dependent actin remodeling and MAL/SRF signaling in keratinocytes, which in turn promotes differentiation via regulation of desmoglein-1 expression.

Cited by 37 publications

References 75 publications

Desmosome regulation and signaling in disease

Desmosome regulation and signaling in disease

Desmosomes: Regulators of Cellular Signaling and Adhesion in Epidermal Health and Disease

Effect of purified fractions from cell culture supernate of high‐density pre‐B acute lymphoblastic leukemia cells (ALL3) on the growth of ALL3 cells at low density

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