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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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CREB3 — MYLIP

Text-mined interactions from Literome

Cheng et al., Neuron 2007 (MAP Kinase Signaling System) : miR-132 is induced by photic entrainment cues via a MAPK/CREB dependent mechanism, modulates clock-gene expression, and attenuates the entraining effects of light
Pigazzi et al., Cancer Res 2009 (Acute Disease...) : miR-34b restored expression caused cell cycle abnormalities, reduced anchorage independent growth, and altered CREB target gene expression, suggesting its suppressor potential
Shi et al., J Biol Chem 2009 : Additionally, both CLOCK ( circadian locomoter output cycles kaput ) and CREB ( cAMP-response element binding protein-1 ) activated gga-mir-26a expression in vitro
Sandoval et al., Advances in hematology 2009 : And, miR-34b , a microRNA that negative regulates CREB expression, is expressed at lower levels in myeloid leukemia cell lines compared to that of healthy bone marrow
Remenyi et al., Biochem J 2010 : Regulation of the miR-212/132 locus by MSK1 and CREB in response to neurotrophins
Jin et al., J Biol Chem 2012 : Moreover, miR-132 overexpression enhanced cyclic AMP-response element binding protein ( CREB ) phosphorylation via RASA1 ( p120 Ras GTPase activating protein 1 ) down-regulation, whereas miR-132 inhibition attenuated Ang II-induced CREB activation
Tan et al., Proc Natl Acad Sci U S A 2012 (Glioma) : Second, microRNA microarray, ChIP-chip, ChIP-quantitative PCR, and luciferase reporter assays showed that CREB directly binds to the regulatory sequences of mir-23a and enhance the expression of mir-23a
Zhou et al., PloS one 2012 : In addition, we found that miR-222 might regulate the phosphorylation of cAMP response element binding protein ( CREB ) through PTEN, and c-Jun activation might enhance the miR-222 expression
Nahid et al., J Immunol 2013 : The rapid induction of miR-132/-212 was transcription factor CREB dependent , and the sustained expression of miR-132/-212 was responsible for inducing tolerance to subsequent PGN challenge