M
Michael Karin
Researcher at University of California, San Diego
Publications - 753
Citations - 246120
Michael Karin is an academic researcher from University of California, San Diego. The author has contributed to research in topics: IκB kinase & Signal transduction. The author has an hindex of 236, co-authored 704 publications receiving 226485 citations. Previous affiliations of Michael Karin include Sanford-Burnham Institute for Medical Research & University of California, Los Angeles.
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Journal ArticleDOI
p63 induces key target genes required for epidermal morphogenesis
Maranke I. Koster,Daisy Dai,Barbara Marinari,Yuji Sano,Antonio Costanzo,Michael Karin,Dennis R. Roop +6 more
TL;DR: In this article, the authors demonstrate that ΔNp63α proteins are essential for maintaining basement membrane integrity and terminal differentiation of keratinocytes, and identify two target genes that mediate these processes.
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Expression of GHF-1 protein in mouse pituitaries correlates both temporally and spatially with the onset of growth hormone gene activity
TL;DR: The spatial and temporal correlation between the appearance of GHF-1 protein and growth hormone gene activation suggests that GHF, the pituitary-specific transcription factor, is responsible for this very last step in the specialization of somatotrophic cells.
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IκB kinase-α acts in the epidermis to control skeletal and craniofacial morphogenesis
TL;DR: It is postulated that the morphogenetic defects in IKK-α-deficient mice are not caused by reduced NF-κB activity but instead are due to failed epidermal differentiation that disrupts proper epidersmal–mesodermal interactions.
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Regulation of the pituitary-specific homeobox gene GHF1 by cell-autonomous and environmental cues.
TL;DR: Analysis of the GHF1 gene, which encodes a mammalian homeodomain protein specifying expression of the growth hormone (GH) gene in anterior pituitary somatotrophs, indicates that transcription is also controlled by cell-autonomous interactions involving positive autoregulation byGHF1, and environmental cues that modulate the intracellular level of cyclic AMP.
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Targeting of TAK1 by the NF-κB protein Relish regulates the JNK-mediated immune response in Drosophila
Jin Mo Park,Helen Brady,Maria Grazia Ruocco,Huaiyu Sun,DeeAnn Williams,Susan J. Lee,Tomohisa Kato,Normand Richards,Kyle W. H. Chan,Frank Mercurio,Michael Karin,Steven A. Wasserman +11 more
TL;DR: It is found that the Drosophila NF-kappa B protein Relish plays a crucial role in limiting the duration of JNK activation and output in response to Gram-negative infections.