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KRAS activates JNK. 22 / 24
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"Although JNK was initially identified as an HRAS-activated kinase [ xref , xref ], it was later shown that mutated KRAS activates JNK both in vitro and in vivo [ xref , xref ]."
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"It seems that the KRAS activation of JNK has a critical role in the maintenance of the self-renewal and tumor-initiating capacity of pancreatic CSCs/CSLCs."
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"Combined, these data suggest that K-Ras activation of JNK has a critical role in the maintenance of the self-renewal and tumor initiating capacity of pancreatic CSCs and CSLCs."
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"As it was stated earlier, JNK was originally identified as an HRAS-activated kinase [ xref , xref ]; however, later, it was shown that mutated KRAS also activates JNK both in vitro and in vivo [ xref , xref ], and the activation of JNK definitely correlated with the expression of oncogenic NRAS in HT-1080 cells [ xref ]."
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"JNK was originally identified as a kinase activated by H-Ras [XREF_BIBR, XREF_BIBR], but subsequently, it was demonstrated that mutated K-Ras activates JNK in vitro and in vivo [XREF_BIBR, XREF_BIBR]."
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"In addition, although Rac1 is an attractive candidate molecule linking K-Ras and JNK [XREF_BIBR], it still remains to be delineated in this study how K-Ras activates JNK in CSLCs."
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"In addition, oncogenic K-ras expression led to activation of JNK in pancreatic cancer cell lines."
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"The imbalance between ERK and JNK activity caused by activated Ki-Ras could have a crucial role in human colorectal tumorigenesis."
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"KRAS expression led to activation of JNK in pancreatic cancer cell lines."
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"Stress response (p38 and c-Jun N-terminal Kinase (JNK)) and Nuclear Factor-kappa B (NF-κB) pathways are also induced by K-RAS activation, either by interconnection with other activated signaling pathw[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"For example, p38 and JNK can be activated by KRAS signaling and these kinases are more specific for ETS1 than ERG."
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"The significance of JNK activation in pancreatic cancer biology remained unclear, but we have only recently demonstrated that JNK activation by KRas, which is mutationally activated in the majority of pancreatic cancers, plays a key role in the maintenance of self-renewal and tumor initiating capacity of pancreatic CSCs [XREF_BIBR]."
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"Although JNK was initially identified as an HRAS-activated kinase [21,22], it was later shown that mutated KRAS activates JNK both in vitro and in vivo [38,39]."
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"It seems that the KRAS activation of JNK has a critical role in the maintenance of the self-renewal and tumor-initiating capacity of pancreatic CSCs/CSLCs."
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"Hence, it seems the cancer cell death amplifying effect of the JNK inhibitors is specific to the ferroptosis inducers and is not necessarily a common feature in oxidative stress-driven cell deaths.As it was stated earlier, JNK was originally identified as an HRAS-activated kinase [21,22]; however, later, it was shown that mutated KRAS also activates JNK both in vitro and in vivo [38,39], and the activation of JNK definitely correlated with the expression of oncogenic NRAS in HT-1080 cells [23]."
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"Notably, oncogenic K-Ras activated all MAPKs (JNK, ERK and p38); however, only p38 was involved in p47 (phox)-NOX1-dependent ROS generation and consequent transformation."
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"These studies indicate that the pancreatic CSCs are dependent on KRAS activation of JNK ( Okada et al., 2014 )."
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"Taken together, these results suggest that activated Ki-Ras-mediated signals are involved in the SEK1-JNK pathway through a PKC isotype that is distinct from that involved in MEK1/2-ERK activation in human colon cancer cells and independent of phosphoinositol 3-kinase activation, and the imbalance between ERK and JNK activity caused by activated Ki-Ras may play critical roles in human colorectal tumorigenesis."
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"The altered conformational bias may clarify their distinct rates of GTP hydrolysis, nucleotide exchange, and phospholipid selectivity, as well as the different favored effectors; K-Ras interacts with Raf-1 and signals through MAPK and Ral guanine nucleotide dissociation stimulator (RalGDS), whereas K-Ras activates PI3K, c-Jun N-terminal kinase (JNK), p38, and focal adhesion kinase (FAK) pathways (110, 111)."
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"Both the ERK and p38 MAPK pathways, but not JNK, were activated by K-Ras (G12 V) and the proliferation and CAFC formation were mediated via ERK, while differentiation was predominantly mediated via p38 (Fatrai et al., 2011)."
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"Core signaling pathways and processes genetically altered in most pancreatic cancersRegulatory process or pathwayApoptosis DNA damage control Regulation of G1/S transition Hedgehog signaling Homophilic cell adhesion Integrin signaling c-Jun N-terminal kinase signaling KRAS Regulation of invasion GTPase dependent signaling TGF-b signaling WNT and Notch signalingNumber of mutated genes in pathway9 9 19 19 30 24 9 5 46 33 37 29Percentage of tumors with genetic alterations in pathway 100% 83% 100% 100% 79% 67% 96% 100% 92% 79% 100% 100% Data from [7], reproduced with permission from AAAS.as balanced chromosome translocations, inversions and rearrangements on a genome-wide scale, although this has now become possible (Box 2)."
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"These studies indicate that the pancreatic CSCs are dependent on KRAS activation of JNK ( Okada et al., 2014 )."
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