Open AccessLow Levels of Raf Kinase Inhibitory Protein in Growth Hormone-Secreting Pituitary Adenomas Correlate with Poor Response to Octreotide Treatment
Author(s) -
Stine Lyngvi Fougner,
Jens Bollerslev,
Fahim Latif,
John Hald,
T. Lund,
Jon RammPettersen,
Jens Petter Berg
Publication year - 2008
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2007-2272
Subject(s) - acromegaly , somatostatin , octreotide , somatostatin receptor , protein kinase a , mapk/erk pathway , endocrinology , medicine , somatostatin receptor 2 , internalization , cancer research , somatostatin receptor 1 , chemistry , g protein coupled receptor , somatostatin receptor 3 , beta adrenergic receptor kinase , signal transduction , kinase , receptor , biology , hormone , growth hormone , biochemistry
Excessive GH production by pituitary tumors causes acromegaly. Medical treatment of acromegaly with somatostatin analogs (SMSs), like octreotide, is well established, but the clinical effect is variable. One mechanism for octreotide effect is inhibition of the MAPK signaling pathway after binding to the G protein-coupled somatostatin receptor. Nonphosphorylated Raf kinase inhibitory protein (RKIP) binds to and inhibits Raf1 kinase, and thereby attenuates MAPK signaling, whereas phosphorylated RKIP inhibits G protein receptor internalization and degradation due to inhibition of G protein receptor kinase 2.
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