z-logo
open-access-imgOpen Access
Sam68 mediates leptin-stimulated growth by modulating leptin receptor signaling in human trophoblastic JEG-3 cells
Author(s) -
Francisca SánchezJiménez,
Antonio PérezPérez,
Carmen González-Yanes,
Cecilia Varone,
Vı́ctor Sánchez-Margalet
Publication year - 2011
Publication title -
human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.446
H-Index - 226
eISSN - 1460-2350
pISSN - 0268-1161
DOI - 10.1093/humrep/der187
Subject(s) - leptin receptor , leptin , signal transduction , phosphorylation , tyrosine phosphorylation , biology , microbiology and biotechnology , gene knockdown , endocrinology , mapk/erk pathway , medicine , cell culture , genetics , obesity
Sam68, a member of the signal transduction and activation of RNA metabolism (STAR) family of RNA-binding proteins, has been previously implicated as an adaptor molecule in different signaling systems, including leptin receptor (LEPR) signaling. LEPR activation is known to stimulate JAK-STAT, MAPK and PI3K signaling pathways, thus mediating the biological effects of leptin in different cell types, including trophoblastic cells. We have recently found that leptin stimulation also promotes the overexpression and tyrosine phosphorylation of Sam68 in human trophoblastic JEG-3 cells, suggesting a role for Sam68 in leptin signaling and action in these cells. In the present work, we have studied the participation of Sam68 in the main signaling pathways activated by LEPR to increase growth and proliferation in trophoblastic JEG-3 cells.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom