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Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition [bulkRNA-seq]

ABSTRACT: Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition [bulkRNA-seq]

PROVIDER: PRJNA993122 | ENA |

REPOSITORIES: ENA

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Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition

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Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition

Project description:Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition

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Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition [scRNA-seq]

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Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition [bulkRNA-seq]

Project description:Comparative gene expression profiling analysis of bulk RNA-seq data for control 501mel cells compared to transient knockdown with two different TBX3 siRNAs

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Loss of MC1R signaling implicates TBX3 in pheomelanogenesis and melanoma predisposition

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Project description:We used single-cell RNA-sequencing (scRNA-seq) of melanocytes isolated from two distict red hair color (RHC) mouse models for comparison with and black hair color, functional MC1R signaling, to reveal a Pheomelanin Gene Signature (PGS) of differentially expressed genes in RHC melanocytes.

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Project description:This SuperSeries is composed of the SubSeries listed below.

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MC1R stabilize the actin cytoskeleton

Project description:Amplification of the Melanocortin-1 Receptor in Nephrotic Syndrome Renders a Good Target for Podocyte Cytoskeleton Stabilization During the last years, several reports have been presented of beneficial effects of ACTH in patients with nephrotic syndrome. Among the known ACTH receptors, the melanocortin-1 receptor (MC1R) has been suggested as the mediator of the ACTH renoprotective effect with the mechanism of action resulting in stabilization of the actin cytoskeleton in podocytes. To understand how melanocortin receptors are regulated in nephrotic syndrome and how they are involved in restoration of filtration barrier function, melanocortin receptor expression was evaluated in patients and in a rat model of nephrotic syndrome in combination with cell culture analysis. Phosphoproteomic mass spectrometry was applied and identified MC1R pathways confirmed using biochemical analysis. We found that glomerular MC1R expression was increased in nephrotic syndrome, both in humans and in a rat model. A MC1R agonist protected podocytes from protamine sulfate induced stress fiber loss with the top ranked phoshoproteomic MC1R activated pathway beeing actin cytoskeleton signaling. Actin stabilization through the MC1R consisted of ERK1/2 dependent phosphorylation and inactivation of EGFR signaling with stabilization of synaptopodin and stress fibers in podocytes. These results further explain how patients with nephrotic syndrome show responsiveness to ACTH treatment by depressing EGFR signaling through activation of the MC1R receptor and as a consequence restore filtration barrier function by stabilizing the podocyte actin cytoskeleton.

2019-11-12 | PXD009198 | Pride

Basal Epidermis from UVB-irradiated Mc1r and Kit mutants

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MC1R Basis of Melanoma - Parkinson’s Link and Neuroprotective Potential of MC1R

Project description:MC1R Basis of Melanoma - Parkinson’s Link and Neuroprotective Potential of MC1R

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