GTPase KRas
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'''GTPase KRas''' (KRas) plays a critical role in the control of cellular growth. Kras stands for Kirsten rat sarcoma virus gene. KRas is a small GTPase that functions as molecular switches by alternating | '''GTPase KRas''' (KRas) plays a critical role in the control of cellular growth. Kras stands for Kirsten rat sarcoma virus gene. KRas is a small GTPase that functions as molecular switches by alternating | ||
between inactive GDP-bound state and active GTP-bound state<ref>PMID:2406906</ref>. | between inactive GDP-bound state and active GTP-bound state<ref>PMID:2406906</ref>. | ||
| + | '''KRas4A''' and '''KRas4B''' are two isoforms of KRas differing in 15 residues which are involved in trafficking and in membrane localisation<ref>PMID:38354232</ref>. | ||
== Disease == | == Disease == | ||
| - | A single mutation of KRas G12C activates KRas and is implicated with various malignancies including lung adenocarcinoma, mutinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma<ref>PMID:29187496</ref>. KRas mutations are the most common genetic abnormalities in cancer. | + | A single mutation of '''KRas G12C''' or '''KRas G12V''' activates KRas and is implicated with various malignancies including lung adenocarcinoma, mutinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma<ref>PMID:29187496</ref>. KRas mutations are the most common genetic abnormalities in cancer. |
== Relevance == | == Relevance == | ||
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</StructureSection> | </StructureSection> | ||
| - | == 3D Structures of GTPase KRas == | ||
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| - | Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}} | ||
| - | {{#tree:id=OrganizedByTopic|openlevels=0| | ||
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| - | *GTPase KRas | ||
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| - | **[[5uk9]] – hKRas + GCP + GDP – human <br /> | ||
| - | **[[5vq2]] – hKRas + GTP <br /> | ||
| - | **[[6god]] – hKRas + GPPNP <br /> | ||
| - | **[[6goe]], [[6gof]], [[6gog]], [[6gom]] – hKRas (mutant) + GPPNP <br /> | ||
| - | **[[5w22]], [[4obe]], [[4lpk]], [[5vq8]] – hKRas + GDP <br /> | ||
| - | **[[3gft]] – hKRas (mutant) + GTP analog <br /> | ||
| - | **[[4l8g]], [[4ldj]], [[4ql3]], [[4tq9]], [[4tqa]], [[6asa]], [[6ase]], [[5whd]], [[5uqw]], [[5us4]], [[5vp7]], [[5vq0]], [[5vq1]], [[4wa7]], [[4lrw]], [[6bof]] – hKRas (mutant) + GDP <br /> | ||
| - | **[[5vpi]], [[5vpz]], [[5vq6]] – hKRas (mutant) + GTP <br /> | ||
| - | **[[5usj]], [[5vpy]] – hKRas (mutant) + GNP <br /> | ||
| - | **[[6bp1]], [[4dsn]] – hKRas (mutant) + GCP <br /> | ||
| - | **[[4dso]] – hKRas (mutant) + inhibitor + GSP <br /> | ||
| - | **[[4dst]] – hKRas (mutant) + inhibitor + GCP <br /> | ||
| - | **[[5kyk]] – hKRas + inhibitor <br /> | ||
| - | **[[4nmm]] – hKRas (mutant) + inhibitor <br /> | ||
| - | **[[5v9o]], [[5f2e]], [[5v9u]], [[4dsu]], [[4luc]], [[4lv6]], [[4lyf]], [[4lyh]], [[4lyj]], [[4m1o]], [[4m1s]], [[4m1t]], [[4m1w]], [[4m1y]], [[4m21]], [[4m22]], [[4epr]], [[4ept]], [[4epv]], [[4epw]], [[4epx]], [[4epy]], [[4q01]], [[4q02]], [[4q03]], [[5vbm]], [[5v6s]], [[5v6v]], [[6ark]], [[5xco]], [[6b0v]], [[6b0y]], [[5yxz]], [[5yy1]], [[4pzy]], [[4pzz]], [[6n2j]], [[6n2k]] – hKRas (mutant) + GDP + inhibitor <br /> | ||
| - | **[[5vbz]], [[6gqy]], [[6gqw]], [[6gqx]], [[6gqt]] – hKRas (mutant) + GNP + inhibitor <br /> | ||
| - | **[[6fa1]], [[6fa2]], [[6fa3]], [[6fa4]], [[5oct]], [[5oco]], [[5ocg]] – hKRas (mutant) + GNP + inhibitor<br /> | ||
| - | **[[6f76]] – hKRas (mutant) + GPPNP + inhibitor<br /> | ||
| - | **[[5v71]], [[5v9l]] – hKRas (mutant) + GDP + quinazoline inhibitor <br /> | ||
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| - | *GTPase KRas complex with protein | ||
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| - | **[[5wha]], [[5whb]] – hKRas (mutant) + miniprotein + GDP <br /> | ||
| - | **[[5wpl]], [[5whe]], [[5wpm]], [[5wlb]] – hKRas (mutant) + miniprotein + GNP <br /> | ||
| - | **[[6h46]] – hKRas + darpin K13 + GDP <br /> | ||
| - | **[[6h47]] – hKRas + darpin K19 <br /> | ||
| - | **[[5o2s]], [[5mlb]] – hKRas + darpin K27 + GDP <br /> | ||
| - | **[[5tb5]], [[5tar]] – hKRas + GMP-PDE d + farnesyl + GDP <br /> | ||
| - | **[[5o2t]], [[5mla]] – hKRas + darpin 55 + GSP <br /> | ||
| - | **[[5ufe]] – hKRas + R11.1.6 + GNP <br /> | ||
| - | **[[5ufq]] – hKRas (mutant) + R11.1.6 + GNP <br /> | ||
| - | **[[2msc]], [[2msd]] – hKRas + apolipoprotein + GDP - NMR<br /> | ||
| - | **[[2mse]] – hKRas + apolipoprotein + A-Raf + GDP - NMR<br /> | ||
| - | **[[6ccx]], [[6cch]], [[6cc9]] – hKRas (mutant) + apolipoprotein + inhibitor + GPPNP - NMR<br /> | ||
| - | **[[6epl]] – hKRas (mutant) + son of sevenless homolog 1<br /> | ||
| - | **[[6epm]], [[6epn]], [[6epo]], [[6epp]] – hKRas (mutant) + son of sevenless homolog 1 + inhibitor<br /> | ||
| - | }} | ||
== References == | == References == | ||
<references/> | <references/> | ||
[[Category:Topic Page]] | [[Category:Topic Page]] | ||
Current revision
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References
- ↑ Milburn MV, Tong L, deVos AM, Brunger A, Yamaizumi Z, Nishimura S, Kim SH. Molecular switch for signal transduction: structural differences between active and inactive forms of protooncogenic ras proteins. Science. 1990 Feb 23;247(4945):939-45. PMID:2406906
- ↑ Whitley MJ, Tran TH, Rigby M, Yi M, Dharmaiah S, Waybright TJ, Ramakrishnan N, Perkins S, Taylor T, Messing S, Esposito D, Nissley DV, McCormick F, Stephen AG, Turbyville T, Cornilescu G, Simanshu DK. Comparative analysis of KRAS4a and KRAS4b splice variants reveals distinctive structural and functional properties. Sci Adv. 2024 Feb 16;10(7):eadj4137. PMID:38354232 doi:10.1126/sciadv.adj4137
- ↑ Shibata H, Ohike N, Norose T, Isobe T, Suzuki R, Imai H, Shiokawa A, Aoki T, Murakami M, Mizukami H, Tanaka JI, Takimoto M. Mucinous Cystic Neoplasms Lined by Abundant Mucinous Epithelium Frequently Involve KRAS Mutations and Malignant Progression. Anticancer Res. 2017 Dec;37(12):7063-7068. doi: 10.21873/anticanres.12178. PMID:29187496 doi:http://dx.doi.org/10.21873/anticanres.12178
- ↑ Sun Q, Burke JP, Phan J, Burns MC, Olejniczak ET, Waterson AG, Lee T, Rossanese OW, Fesik SW. Discovery of Small Molecules that Bind to K-Ras and Inhibit Sos-Mediated Activation. Angew Chem Int Ed Engl. 2012 May 8. doi: 10.1002/anie.201201358. PMID:22566140 doi:10.1002/anie.201201358
