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1 CRMP2) in ILK-deficient melanocytes restored dendricity.
2 tes, and Ilk inactivation reduces melanocyte dendricity.
3 e to sPLA2-X activity, stimulates melanocyte dendricity.
4 late both tyrosinase activity and melanocyte dendricity.
5 paracrine factors that stimulate melanocyte dendricity.
6 ing contribute to PGE(2)-mediated melanocyte dendricity.
7 rradiation, a potent stimulus for melanocyte dendricity.
8 a (PKCzeta) activity abrogated LPC-dependent dendricity.
9 ns that upon activation stimulate melanocyte dendricity and activity of tyrosinase, a key enzyme in m
13 diated skin, an increase in melanocyte size, dendricity, and number, as well as increased pigment in
16 levels, gp100 protein expression, melanocyte dendricity, and the number gp100+ HF melanocytes, were a
23 or agonists resulted in increased melanocyte dendricity, indicating that both EP1 and EP3 receptor si
24 vated cAMP in human melanocytes showing that dendricity observed in response to PGE(2) and PGF(2alpha
27 guidance, stimulates melanocyte adhesion and dendricity through opposing actions of beta1-integrin an