A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

IndraLab

Statements

databases
phosphosite cbn pc11 biopax bel_lc signor biogrid tas lincs_drug hprd trrust | geneways tees isi trips rlimsp medscan sparser reach
reading

NRAS activates KRAS. 5 / 5
| 5
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"Noteably, NRAS knockdown further enhanced inhibition of proliferation in the absence of KRAS (XREF_FIG D)."
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"It is also possible that NRAS may activate different signaling pathways to KRAS and HRAS; an idea supported by the observation that NRAS has greater transforming activity than KRAS in experimental models of melanoma."
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"In contrast to nonresistant cells, NRAS inhibition alone was sufficient to significantly impair proliferation in resistant cells, and NRAS knockdown only slightly and nonsignificantly induced KRAS upregulation."
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"Taken together, these results show that signaling by H-Ras and N-Ras, but not K-Ras, are required to promote PGA 1 -induced apoptosis."
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"Such Raichu-KRas probe has been recently used to document the specific activation of K-Ras but not H-Ras or N-Ras on late endosomes thus identifying a mechanism for intracellular signal propagation [XREF_BIBR]."
NRAS activates mutated KRAS. 3 / 3
| 3
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"Deletion of Hras or Nras increased the number of mutant Kras driven lung tumors, suggesting that Hras and Nras attenuate the ability of mutant Kras to promote lung carcinogenesis."
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"Another study highlighted the importance of wild-type RAS proteins by revealing that wild-type HRAS and NRAS promote mutant KRAS driven tumorigenesis XREF_BIBR."
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"Wild-type H- and N-Ras promote mutant K-Ras driven tumorigenesis by modulating the DNA damage response."
Mutated NRAS activates KRAS. 1 / 1
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"Recent studies revealed that " minor " activating mutations such as those in KRAS codons 61 and 146, as well as NRAS mutations, contribute to resistance."