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Receptor-interacting serine-threonine kinase 4

The protein encoded by this gene is a serine/threonine protein kinase that interacts with protein kinase C-delta. The encoded protein can also activate NFkappaB and is required for keratinocyte differentiation. This kinase undergoes autophosphorylation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Kallikrein, ACID, CAN, cytokeratin, HAD
Papers on PKK
Effect of interleukin-17 on receptor-interacting protein 4 expression and keratinocyte proliferation.
Sun et al., Jinan, China. In Exp Ther Med, Jul 2015
UNASSIGNED: The aim of the present study was to investigate the effect of receptor-interacting protein 4 (RIP4) on keratinocyte proliferation and its role in the pathogenesis of psoriasis vulgaris.
PKK suppresses tumor growth and is decreased in squamous cell carcinoma of the skin.
Chen et al., Rochester, United States. In J Invest Dermatol, Mar 2015
The current study identifies the protein kinase C-associated kinase (PKK), which is also known as the receptor-interacting protein kinase 4, as a suppressor of tumor growth in SCC of the skin.
Correction: Virtual screening and optimization of Type II inhibitors of JAK2 from a natural product library.
Leung et al., Hong Kong, Hong Kong. In Chem Commun (camb), Feb 2015
Correction for 'Virtual screening and optimization of Type II inhibitors of JAK2 from a natural product library' by Dik-Lung Ma et al., Chem.
Protein kinase C-associated kinase regulates NF-κB activation through inducing IKK activation.
Chen et al., Pusan, South Korea. In Int J Oncol, 2014
We previously showed that protein kinase C-associated kinase (PKK, also known as DIK/RIP4), which belongs to the receptor-interacting protein (RIP) kinase family, mediates the B cell activating factor of the TNF family (BAFF)-induced NF-κB activation in diffuse large B cell lymphoma (DLBCL) cell lines.
Inhibition of vascular permeability by antisense-mediated inhibition of plasma kallikrein and coagulation factor 12.
MacLeod et al., Carlsbad, United States. In Nucleic Acid Ther, 2013
Our studies demonstrate that ASO-mediated reduction in C1-INH plasma levels results in increased vascular permeability and that inhibition of proteases of the kinin-kallikrein system, either f12 or prekallikrein (PKK) reverse the effects of C1-INH depletion with similar effects on both basal and angiotensin converting enzyme (ACE) inhibitor-induced permeability.
Exome sequence identifies RIPK4 as the Bartsocas-Papas syndrome locus.
Dixon et al., Manchester, United Kingdom. In Am J Hum Genet, 2012
The present study's findings show that recessive mutations in RIPK4 cause Bartsocas-Papas syndrome and its variant, the autosomal-recessive form of multiple pterygium syndrome (Aslan type).
Selective depletion of plasma prekallikrein or coagulation factor XII inhibits thrombosis in mice without increased risk of bleeding.
MacLeod et al., Carlsbad, United States. In Blood, 2011
We demonstrate that selective reduction of prekallikrein (PKK), another member of the contact system, using antisense oligonucleotide (ASO) technology results in an antithrombotic phenotype in mice.
cIAP1/2 are direct E3 ligases conjugating diverse types of ubiquitin chains to receptor interacting proteins kinases 1 to 4 (RIP1-4).
Vandenabeele et al., Gent, Belgium. In Plos One, 2010
In this study, we found that XIAP, cIAP1 and cIAP2 not only directly bind to RIP1 and RIP2 but also to RIP3 and RIP4.
RIP2: a novel player in the regulation of keratinocyte proliferation and cutaneous wound repair?
Munz et al., Berlin, Germany. In Exp Cell Res, 2010
We could recently demonstrate an important role of receptor interacting protein 4 (RIP4) in the regulation of keratinocyte differentiation.
RIP4 is a target of multiple signal transduction pathways in keratinocytes: implications for epidermal differentiation and cutaneous wound repair.
Munz et al., Berlin, Germany. In Exp Cell Res, 2010
Data indicate that rip4 gene expression is regulated in a complex manner, which might have therapeutic implications.
RIP4 regulates epidermal differentiation and cutaneous inflammation.
Holland et al., Seattle, United States. In J Invest Dermatol, 2010
RIP4 functions in the epidermis through PKC-specific signaling pathways to regulate differentiation and inflammation
Novel PKC signaling is required for LPS-induced soluble Flt-1 expression in macrophages.
Tsao et al., Taipei, Taiwan. In J Leukoc Biol, 2008
Phosphorylation of protein kinase C delta is associated with activation of vascular endothelial growth factor and soluble fms-like tyrosine kinase-1 receptor in lipopolysaccharide induced macrophages
Transforming growth factor-beta-mediated regulation of BK virus gene expression.
Imperiale et al., Ann Arbor, United States. In Virology, 2008
Promoter activity is upregulated in the presence of TGF-beta for the TU strain of BKV, and not for the Dik, Dunlop, or Proto-2 strains.
Protein kinase C-associated kinase is required for NF-kappaB signaling and survival in diffuse large B-cell lymphoma cells.
Zhao et al., Rochester, United States. In Blood, 2008
PKK plays a pivotal role in the survival of human Diffuse large B-cell lymphoma (DLBCL) cells and represents a potential target for DLBCL therapy
Study on the biochemical characterization of herbicide detoxification enzyme, glutathione S-transferase.
Kong et al., Seoul, South Korea. In Biofactors, 2006
In this study, the genes of the plant specific phi and tau class GST enzymes from Oryza sativa (OsGST) and human pi class GST enzyme (hGSTP1-1) were cloned and expressed in Escherichia coli with the pET and pKK vector systems, respectively.
True pulmonary carcinosarcoma (squamous cell carcinoma and chondrosarcoma). A case report.
Fukui et al., Tottori, Japan. In Acta Pathol Jpn, 1992
Immunohistochemically, the cytoplasm of numerous cells of the squamous cell carcinoma component was stained with anti-cytokeratin (PKK 1) and the cytoplasmic membrane with anti-epithelial membrane antigen (EMA).
Continuous Immobilized Recombinant Protein Production from E. coli Capable of Selective Protein Excretion: A Feasibility Study.
Wilson et al., Ithaca, United States. In Biotechnol Prog, 1985
To test this concept we have used plasmid pKK in E. coli RB791 with beta-lactamase as the target protein.
[Role of the kallikrein-kininogen-kinin system in the inflammatory reaction and septic shock].
Adam et al., In Ann Biol Clin (paris), 1983
Two studies of experimental endotoxemia in burns patients, septicemia and septic shock have demonstrated the following facts: activation occurs of specific ( pKK ) and non-specific (plasminogen-plasmin system) kininogenases , K-HMW and K-LMW levels are significantly decreased.
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