IndraLab

Statements

CYLD activates JNK. 13 / 13
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"CYLD Inhibits Tumorigenesis and Metastasis by Blocking JNK and AP1 Signaling at Multiple Levels."
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"Also, CYLD knocking-out macrophages could increase JNK activity through ubiquitinizing TRAF-2 protein, and studies have confirmed that CYLD knocking-out mice were prone to cancers [11, 12]."
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"In agreement with the reported negative regulation of JNK and c-Myc activation by CYLD [XREF_BIBR], WB analysis of these molecules showed increased Akt, JNK and c-Myc activation (measured as levels of P-Akt, P-JNK and P-c-Myc respectively) in the skin of transgenic mice lacking the DUB function (XREF_FIG)."
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"Moreover, we found that CYLD m not only increased JNK activity but also increased K63 ubiqutination on both c-Jun and c-Fos, and ultimately potentiated AP1 transcriptional activity."
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"Curiously, in CD3+ CD28 stimulated Jurkat T cells, MALT1 cleaves CYLD increasing activation of JNK, but not NF-kappaB [XREF_BIBR]."
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"[76] W. Reiley, M. Zhang, and S.C. Sun, Negative regulation of JNK signaling by the tumor suppressor CYLD."
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"2 The inhibition of CYLD function in keratinocytes enhances the activation of the JNK pathway."
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"In addition, orthologs of genes involved in JNK signaling, such as bendless, Pvr, Alg-2, CYLD, cpa, and Cdc42 [51, 52, 53, 54, 55, 56, 57], were highly expressed by MGHs."
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"In support of this view, MALT1 proteolysis of the inhibitory deubiquitinases A20 and CYLD potentiates NF-kappaB and JNK, respectively [XREF_BIBR, XREF_BIBR], while cleavage of the RNase Regnase-1 prolongs mRNA stability of T cell effector genes [XREF_BIBR]."
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"We show that mesenchymal Cyld contributes to prevent excessive JNK and NF-κB activation in TNF-stimulated naive and arthritic SFs."
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"Tumor suppressor CYLD, a ubiquitin-editing enzyme, can negatively regulate the NF-κB and JNK signaling pathways by removing Lys63-linked ubiquitin chains from its target proteins (like TRAF2/6 and NEMO)."
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"MALT1 cleaves Bcl-10, deubiquitinases A20 and CYLD, and NF-κB subunit RelB, thereby modulating NF-κB and JNK signaling (18–21)."
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"In agreement with the reported negative regulation of JNK and c-Myc activation by CYLD [ xref ], WB analysis of these molecules showed increased Akt, JNK and c-Myc activation (measured as levels of P-Akt, P-JNK and P-c-Myc respectively) in the skin of transgenic mice lacking the DUB function ( xref )."
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