Melanocyte fate in neural crest is triggered by Myb proteins through activation of c-kit

Karafiát, Vı́t; Dvořáková, M; Pajer, Petr; Čermák, Vladimı́r; Dvořák, Michal

doi:10.1007/s00018-007-7330-5

Cited by 15 publications

(13 citation statements)

References 58 publications

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“…Thus, signaling pathways mediated by Wnts, FGFs, BMPs, c-Myb, and msh homeobox 1 (Msx-1) conspire to induce EMT (38)(39)(40). Among them, BMP most prominently induces the migratory property of neural crest cells.…”

Section: Type 1 Emt: Emt During Implantation Embryogenesis and Orgamentioning

confidence: 99%

The basics of epithelial-mesenchymal transition

Kalluri¹,

Weinberg²

2009

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The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

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Section: Type 1 Emt: Emt During Implantation Embryogenesis and Orgamentioning

confidence: 99%

The basics of epithelial-mesenchymal transition

Kalluri¹,

Weinberg²

2009

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“…A reporter construct containing the Kit promoter was activated when cotransfected with a MYB expression vector, providing further evidence of a role for Myb in the regulation of KIT (Hogg et al 1997). Overexpression of the proto-oncogene c-MYB in avian neural crest cells increased KIT and subsequent KITL-KIT signalling, transforming these cells into melanocytes and thereby establishing a role for c-MYB in KIT regulation (Karafiat et al 2007). Similarly, c-MYB knockdown in normal erythroid progenitor cells demonstrated that c-MYB is required for KIT expression in erythroid cells (Vegiopoulos et al 2006).…”

Section: Myb and Etsmentioning

confidence: 97%

Control of KIT signalling in male germ cells: what can we learn from other systems?

Mithraprabhu¹,

Loveland²

2009

Reproduction

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The KIT ligand (KITL)/KIT-signalling system is among several pathways known to be essential for fertility. In the postnatal testis, the KIT/KITL interaction is crucial for spermatogonial proliferation, differentiation, survival and subsequent entry into meiosis. Hence, identification of endogenous factors that regulate KIT synthesis is important for understanding the triggers driving germ cell maturation. Although limited information is available regarding local factors in the testicular microenvironment that modulate KIT synthesis at the onset of spermatogenesis, knowledge from other systems could be used as a basis for identifying how KIT function is regulated in germ cells. This review describes the known regulators of KIT, including transcription factors implicated in KIT promoter regulation. In addition, specific downstream outcomes in biological processes that KIT orchestrates are addressed. These are discussed in relationship to current knowledge of mammalian germ cell development.

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“…In the colon, c-Myb is required for colonic crypt homeostasis, including the integrity, normal differentiation, and steady-state proliferation of colon epithelial stem cells and progenitors (48, 55, 56). Interestingly, c-Myb expression has been found to be important for neural progenitor cell proliferation and for maintenance of neural stem cell niche (57), and an involvement of c-Myb in melanocytes links it to the functions of neural crest cells (44). Clearly, the c- myb gene is widely expressed, and the c-Myb protein plays a role in many cell types, not just hematopoietic cells.…”

Section: The Two Faces Of Myb: a Regulator And An Oncogenementioning

confidence: 99%

“…However, evidence of transformation by the v-Myb proteins is restricted to hematopoietic (157) and some neural crest cells (44). Since Myb proteins are transcription factors, the oncogenic activity is presumably linked to the activation or repression of specific target genes.…”

Section: Does Myb Regulate Differentiation Proliferation or Both?mentioning

confidence: 99%

Myb proteins: angels and demons in normal and transformed cells

Zhou

Ness²

2011

Front Biosci

108

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A key regulator of proliferation, differentiation and cell fate, the c-Myb transcription factor regulates the expression of hundreds of genes and is in turn regulated by numerous pathways and protein interactions. However, the most unique feature of c-Myb is that it can be converted into an oncogenic transforming protein through a few mutations that completely change its activity and specificity. The c-Myb protein is a myriad of interactions and activities rolled up in a protein that controls proliferation and differentiation in many different cell types. Here we discuss the background and recent progress that have led to a better understanding of this complex protein, and outline the questions that have yet to be answered.

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Melanocyte fate in neural crest is triggered by Myb proteins through activation of c-kit

Cited by 15 publications

References 58 publications

The basics of epithelial-mesenchymal transition

The basics of epithelial-mesenchymal transition

Control of KIT signalling in male germ cells: what can we learn from other systems?

Myb proteins: angels and demons in normal and transformed cells

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