Sökning: WFRF:(Raso C.) > Extensive rewiring ...
Fältnamn | Indikatorer | Metadata |
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000 | 03955naa a2200805 4500 | |
001 | oai:DiVA.org:kth-267770 | |
003 | SwePub | |
008 | 200304s2020 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-2677702 URI |
024 | 7 | a https://doi.org/10.1038/s41467-019-14224-92 DOI |
040 | a (SwePub)kth | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Kennedy, S. A.4 aut |
245 | 1 0 | a Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRASG13D |
264 | c 2020-01-24 | |
264 | 1 | b Springer Nature,c 2020 |
338 | a print2 rdacarrier | |
500 | a QC 20200304 | |
520 | a Protein-protein-interaction networks (PPINs) organize fundamental biological processes, but how oncogenic mutations impact these interactions and their functions at a network-level scale is poorly understood. Here, we analyze how a common oncogenic KRAS mutation (KRASG13D) affects PPIN structure and function of the Epidermal Growth Factor Receptor (EGFR) network in colorectal cancer (CRC) cells. Mapping >6000 PPIs shows that this network is extensively rewired in cells expressing transforming levels of KRASG13D (mtKRAS). The factors driving PPIN rewiring are multifactorial including changes in protein expression and phosphorylation. Mathematical modelling also suggests that the binding dynamics of low and high affinity KRAS interactors contribute to rewiring. PPIN rewiring substantially alters the composition of protein complexes, signal flow, transcriptional regulation, and cellular phenotype. These changes are validated by targeted and global experimental analysis. Importantly, genetic alterations in the most extensively rewired PPIN nodes occur frequently in CRC and are prognostic of poor patient outcomes. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng |
700 | 1 | a Jarboui, M. -A4 aut |
700 | 1 | a Srihari, S.4 aut |
700 | 1 | a Raso, C.4 aut |
700 | 1 | a Bryan, K.4 aut |
700 | 1 | a Dernayka, L.4 aut |
700 | 1 | a Charitou, T.4 aut |
700 | 1 | a Bernal-Llinares, M.4 aut |
700 | 1 | a Herrera-Montavez, C.4 aut |
700 | 1 | a Krstic, A.4 aut |
700 | 1 | a Matallanas, D.4 aut |
700 | 1 | a Kotlyar, M.4 aut |
700 | 1 | a Jurisica, I.4 aut |
700 | 1 | a Curak, J.4 aut |
700 | 1 | a Wong, V.4 aut |
700 | 1 | a Stagljar, I.4 aut |
700 | 1 | a LeBihan, T.4 aut |
700 | 1 | a Imrie, L.4 aut |
700 | 1 | a Pillai, P.4 aut |
700 | 1 | a Lynn, M. A.4 aut |
700 | 1 | a Fasterius, Erik,d 1987-u KTH,Systembiologi4 aut0 (Swepub:kth)u1suoteg |
700 | 1 | a Al-Khalili Szigyarto, Cristinau KTH,Skolan för kemi, bioteknologi och hälsa (CBH),Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:kth)u1c02mh9 |
700 | 1 | a Breen, J.4 aut |
700 | 1 | a Kiel, C.4 aut |
700 | 1 | a Serrano, L.4 aut |
700 | 1 | a Rauch, N.4 aut |
700 | 1 | a Rukhlenko, O.4 aut |
700 | 1 | a Kholodenko, B. N.4 aut |
700 | 1 | a Iglesias-Martinez, L. F.4 aut |
700 | 1 | a Ryan, C. J.4 aut |
700 | 1 | a Pilkington, R.4 aut |
700 | 1 | a Cammareri, P.4 aut |
700 | 1 | a Sansom, O.4 aut |
700 | 1 | a Shave, S.4 aut |
700 | 1 | a Auer, M.4 aut |
700 | 1 | a Horn, N.4 aut |
700 | 1 | a Klose, F.4 aut |
700 | 1 | a Ueffing, M.4 aut |
700 | 1 | a Boldt, K.4 aut |
700 | 1 | a Lynn, D. J.4 aut |
700 | 1 | a Kolch, W.4 aut |
710 | 2 | a KTHb Systembiologi4 org |
773 | 0 | t Nature Communicationsd : Springer Natureg 11:1q 11:1x 2041-1723 |
856 | 4 | u https://doi.org/10.1038/s41467-019-14224-9y Fulltext |
856 | 4 | u https://www.nature.com/articles/s41467-019-14224-9.pdf |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-267770 |
856 | 4 8 | u https://doi.org/10.1038/s41467-019-14224-9 |
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