Deficiency of 14-3-3ϵ and 14-3-3ζ by the Wnt1 promoter-driven Cre recombinase results in pigmentation defects

被引：7

作者：

Cornell B. ^{[1
]}

Toyo-Oka K. ^{[1
]}

机构：

[1] Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, 19129, PA

来源：

BMC Research Notes | / 9卷 / 1期

关键词：

14-3-3; Cre transgenic mouse; Knockout mouse; Melanocyte; Neural crest cell; Pigmentation; Weight modulation; White patch; Ywhae; Ywhaz;

D O I：

10.1186/s13104-016-1980-z

中图分类号：

学科分类号：

摘要：

Background: The seven 14-3-3 protein isoforms bind to numerous proteins and are involved in a wide variety of cellular events, including the cell cycle, cell division, apoptosis and cancer. We previously found the importance of 14-3-3 proteins in neuronal migration of pyramidal neurons in the developing cortex. Here, we test the function of 14-3-3 proteins in the development of neural crest cells in vivo using mouse genetic approaches. Results: We found that 14-3-3 proteins are important for the development of neural crest cells, in particular for the pigmentation of the fur on the ventral region of mice. Conclusions: Our data obtained from the 14-3-3ϵ/14-3-3ζ/Wnt1-Cre mice strongly indicate the importance of 14-3-3 proteins in the development of melanocyte lineages. © 2016 Cornell and Toyo-oka.

引用

共 32 条

[1]

Yaffe M.B., How do 14-3-3 proteins work? - Gatekeeper phosphorylation and the molecular anvil hypothesis, FEBS Lett, 513, 1, pp. 53-57, (2002)

[2]

Toyo-Oka K., Wachi T., Hunt R.F., Baraban S.C., Taya S., Ramshaw H., Et al., 14-3-3ϵ and ζ regulate neurogenesis and differentiation of neuronal progenitor cells in the developing brain, J Neurosci, 34, 36, pp. 12168-12181, (2014)

[3]

Toyo-Oka K., Shionoya A., Gambello M.J., Cardoso C., Leventer R., Ward H.L., Et al., 14-3-3epsilon is important for neuronal migration by binding to NUDEL: A molecular explanation for Miller-Dieker syndrome, Nat Genet, 34, 3, pp. 274-285, (2003)

[4]

Cheah P.S., Ramshaw H.S., Thomas P.Q., Toyo-Oka K., Xu X., Martin S., Et al., Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency, Mol Psychiatry., 17, 4, pp. 451-466, (2012)

[5]

Ikeda M., Hikita T., Taya S., Uraguchi-Asaki J., Toyo-Oka K., Wynshaw-Boris A., Et al., Identification of YWHAE, a gene encoding 14-3-3epsilon, as a possible susceptibility gene for schizophrenia, Hum Mol Genet, 17, 20, pp. 3212-3222, (2008)

[6]

Kosaka Y., Cieslik K.A., Li L., Lezin G., Maguire C.T., Saijoh Y., Et al., 14-3-3ϵ plays a role in cardiac ventricular compaction by regulating the cardiomyocyte cell cycle, Mol Cell Biol, 32, 24, pp. 5089-5102, (2012)

[7]

Kleppe R., Martinez A., Doskeland S.O., Haavik J., The 14-3-3 proteins in regulation of cellular metabolism, Semin Cell Dev Biol, 22, 7, pp. 713-719, (2011)

[8]

Hermeking H., The 14-3-3 cancer connection, Nat Rev Cancer, 3, 12, pp. 931-943, (2003)

[9]

Wilker E., Yaffe M.B., 14-3-3 Proteins - A focus on cancer and human disease, J Mol Cell Cardiol, 37, 3, pp. 633-642, (2004)

[10]

Freeman A.K., Morrison D.K., 14-3-3 Proteins: Diverse functions in cell proliferation and cancer progression, Semin Cell Dev Biol, 22, 7, pp. 681-687, (2011)

← 1 2 3 4 →