PIK3CA (Japanese Wikipedia)

Analysis of information sources in references of the Wikipedia article "PIK3CA" in Japanese language version.

refsWebsite

Global rank Japanese rank

36nih.gov

4^th place

24^th place

23doi.org

2^nd place

6^th place

2ensembl.org

1,626^th place

2,625^th place

2wikipedia.org

low place

1zenodo.org

621^st place

4,635^th place

1fda.gov

447^th place

1,043^rd place

doi.org (Global: 2^nd place; Japanese: 6^th place)

“Phosphatidylinositol 3-kinase: structure and expression of the 110 kd catalytic subunit”. Cell 70 (3): 419–29. (August 1992). doi:10.1016/0092-8674(92)90166-A. PMID 1322797.
Rommel, Christian, ed (2010-01-01). “Oncogenic mutations of PIK3CA in human cancers”. Phosphoinositide 3-kinase in Health and Disease. Current Topics in Microbiology and Immunology. 347. Springer Berlin Heidelberg. pp. 21–41. doi:10.1007/82_2010_68. ISBN 9783642148156. PMC 3164550. PMID 20535651
“PIK3CA as an oncogene in cervical cancer”. Oncogene 19 (23): 2739–44. (May 2000). doi:10.1038/sj.onc.1203597. PMID 10851074.
“Role of E542 and E545 missense mutations of PIK3CA in breast cancer: a comparative computational approach”. Journal of Biomolecular Structure & Dynamics 35 (12): 2745–2757. (September 2016). doi:10.1080/07391102.2016.1231082. PMID 27581627.
“PIK3CA mutations in breast cancer: reconciling findings from preclinical and clinical data”. Breast Cancer Research 16 (1): 201. (January 2014). doi:10.1186/bcr3605. PMC 4054885. PMID 25192370.
“Aspirin therapy for colorectal cancer with PIK3CA mutation: simply complex!”. Journal of Clinical Oncology 31 (34): 4358–61. (December 2013). doi:10.1200/jco.2013.52.0080. PMID 24166520.
“High frequency of mutations of the PIK3CA gene in human cancers”. Science 304 (5670): 554. (April 2004). doi:10.1126/science.1096502. PMID 15016963.
“Prospects for phosphoinositide 3-kinase inhibition as a cancer treatment”. Endocrine-Related Cancer (Bioscientifica) 8 (3): 237–48. (September 2001). doi:10.1677/erc.0.0080237. PMID 11566615.
“Targeting phosphoinositide 3-kinase: moving towards therapy”. Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1784 (1): 159–85. (January 2008). doi:10.1016/j.bbapap.2007.10.003. PMID 17997386.
“Aspirin use, tumor PIK3CA mutation, and colorectal-cancer survival”. The New England Journal of Medicine 367 (17): 1596–606. (October 2012). doi:10.1056/nejmoa1207756. PMC 3532946. PMID 23094721.
“Evaluation of PIK3CA mutation as a predictor of benefit from nonsteroidal anti-inflammatory drug therapy in colorectal cancer”. Journal of Clinical Oncology 31 (34): 4297–305. (December 2013). doi:10.1200/jco.2013.50.0322. PMID 24062397. https://zenodo.org/record/3439753. ^{[リンク切れ]}
“Somatic Activating PIK3CA Mutations Cause Venous Malformation”. American Journal of Human Genetics 97 (6): 914–21. (December 2015). doi:10.1016/j.ajhg.2015.11.011. PMC 4678782. PMID 26637981.
“Lymphatic and other vascular malformative/overgrowth disorders are caused by somatic mutations in PIK3CA”. The Journal of Pediatrics 166 (4): 1048–54.e1–5. (April 2015). doi:10.1016/j.jpeds.2014.12.069. PMC 4498659. PMID 25681199.
“Role of E542 and E545 missense mutations of PIK3CA in breast cancer: a comparative computational approach”. Journal of Biomolecular Structure & Dynamics 35 (12): 2745–2757. (September 2016). doi:10.1080/07391102.2016.1231082. PMID 27581627.
“Investigating the Inhibitory Effect of Wortmannin in the Hotspot Mutation at Codon 1047 of PIK3CA Kinase Domain: A Molecular Docking and Molecular Dynamics Approach”. Advances in Protein Chemistry and Structural Biology 102: 267–97. (2016-01-01). doi:10.1016/bs.apcsb.2015.09.008. PMID 26827608.
“Protein kinase Calpha-induced p115RhoGEF phosphorylation signals endothelial cytoskeletal rearrangement”. The Journal of Biological Chemistry 278 (31): 28793–8. (August 2003). doi:10.1074/jbc.M303900200. PMID 12754211.
“Centaurin-alpha(1) associates with and is phosphorylated by isoforms of protein kinase C”. Biochemical and Biophysical Research Communications 307 (3): 459–65. (August 2003). doi:10.1016/s0006-291x(03)01187-2. PMID 12893243.
“Protein kinase C alpha phosphorylates and negatively regulates diacylglycerol kinase zeta”. The Journal of Biological Chemistry 278 (41): 39542–7. (October 2003). doi:10.1074/jbc.M307153200. PMID 12890670.
“The small GTP-binding protein, Rhes, regulates signal transduction from G protein-coupled receptors”. Oncogene 23 (2): 559–68. (January 2004). doi:10.1038/sj.onc.1207161. PMID 14724584.
“The leucine-rich repeat protein SUR-8 enhances MAP kinase activation and forms a complex with Ras and Raf”. Genes & Development 14 (8): 895–900. (April 2000). doi:10.1101/gad.14.8.895. PMC 316541. PMID 10783161.
“Activation of phosphoinositide 3-kinase by interaction with Ras and by point mutation”. The EMBO Journal 15 (10): 2442–51. (May 1996). doi:10.1002/j.1460-2075.1996.tb00602.x. PMC 450176. PMID 8665852.
“The anti-apoptotic effect of Notch-1 requires p56lck-dependent, Akt/PKB-mediated signaling in T cells”. The Journal of Biological Chemistry 279 (4): 2937–44. (January 2004). doi:10.1074/jbc.M309924200. PMID 14583609.
“Phosphatidylinositol (PI) 3-kinase and PI 4-kinase binding to the CD4-p56lck complex: the p56lck SH3 domain binds to PI 3-kinase but not PI 4-kinase”. Molecular and Cellular Biology 13 (12): 7708–17. (December 1993). doi:10.1128/mcb.13.12.7708. PMC 364842. PMID 8246987.

ensembl.org (Global: 1,626^th place; Japanese: 2,625^th place)

May2017.archive.ensembl.org

GRCh38: Ensembl release 89: ENSG00000121879 - Ensembl, May 2017
GRCm38: Ensembl release 89: ENSMUSG00000027665 - Ensembl, May 2017

fda.gov (Global: 447^th place; Japanese: 1,043^rd place)

“FDA approves new treatment for adults with relapsed follicular lymphoma”. US Food and Drug Administration (2017年9月14日). 2023年9月15日閲覧。

nih.gov (Global: 4^th place; Japanese: 24^th place)

pubmed.ncbi.nlm.nih.gov

“Phosphatidylinositol 3-kinase: structure and expression of the 110 kd catalytic subunit”. Cell 70 (3): 419–29. (August 1992). doi:10.1016/0092-8674(92)90166-A. PMID 1322797.
Rommel, Christian, ed (2010-01-01). “Oncogenic mutations of PIK3CA in human cancers”. Phosphoinositide 3-kinase in Health and Disease. Current Topics in Microbiology and Immunology. 347. Springer Berlin Heidelberg. pp. 21–41. doi:10.1007/82_2010_68. ISBN 9783642148156. PMC 3164550. PMID 20535651
“PIK3CA as an oncogene in cervical cancer”. Oncogene 19 (23): 2739–44. (May 2000). doi:10.1038/sj.onc.1203597. PMID 10851074.
“Role of E542 and E545 missense mutations of PIK3CA in breast cancer: a comparative computational approach”. Journal of Biomolecular Structure & Dynamics 35 (12): 2745–2757. (September 2016). doi:10.1080/07391102.2016.1231082. PMID 27581627.
“PIK3CA mutations in breast cancer: reconciling findings from preclinical and clinical data”. Breast Cancer Research 16 (1): 201. (January 2014). doi:10.1186/bcr3605. PMC 4054885. PMID 25192370.
“Aspirin therapy for colorectal cancer with PIK3CA mutation: simply complex!”. Journal of Clinical Oncology 31 (34): 4358–61. (December 2013). doi:10.1200/jco.2013.52.0080. PMID 24166520.
“High frequency of mutations of the PIK3CA gene in human cancers”. Science 304 (5670): 554. (April 2004). doi:10.1126/science.1096502. PMID 15016963.
“Prospects for phosphoinositide 3-kinase inhibition as a cancer treatment”. Endocrine-Related Cancer (Bioscientifica) 8 (3): 237–48. (September 2001). doi:10.1677/erc.0.0080237. PMID 11566615.
“Targeting phosphoinositide 3-kinase: moving towards therapy”. Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1784 (1): 159–85. (January 2008). doi:10.1016/j.bbapap.2007.10.003. PMID 17997386.
“Aspirin use, tumor PIK3CA mutation, and colorectal-cancer survival”. The New England Journal of Medicine 367 (17): 1596–606. (October 2012). doi:10.1056/nejmoa1207756. PMC 3532946. PMID 23094721.
“Evaluation of PIK3CA mutation as a predictor of benefit from nonsteroidal anti-inflammatory drug therapy in colorectal cancer”. Journal of Clinical Oncology 31 (34): 4297–305. (December 2013). doi:10.1200/jco.2013.50.0322. PMID 24062397. https://zenodo.org/record/3439753. ^{[リンク切れ]}
“Somatic Activating PIK3CA Mutations Cause Venous Malformation”. American Journal of Human Genetics 97 (6): 914–21. (December 2015). doi:10.1016/j.ajhg.2015.11.011. PMC 4678782. PMID 26637981.
“Lymphatic and other vascular malformative/overgrowth disorders are caused by somatic mutations in PIK3CA”. The Journal of Pediatrics 166 (4): 1048–54.e1–5. (April 2015). doi:10.1016/j.jpeds.2014.12.069. PMC 4498659. PMID 25681199.
Pagon, Roberta A., ed (1993-01-01). “PIK3CA-Related Overgrowth Spectrum”. PIK3CA-Related Segmental Overgrowth. University of Washington, Seattle. PMID 23946963
“Role of E542 and E545 missense mutations of PIK3CA in breast cancer: a comparative computational approach”. Journal of Biomolecular Structure & Dynamics 35 (12): 2745–2757. (September 2016). doi:10.1080/07391102.2016.1231082. PMID 27581627.
“Investigating the Inhibitory Effect of Wortmannin in the Hotspot Mutation at Codon 1047 of PIK3CA Kinase Domain: A Molecular Docking and Molecular Dynamics Approach”. Advances in Protein Chemistry and Structural Biology 102: 267–97. (2016-01-01). doi:10.1016/bs.apcsb.2015.09.008. PMID 26827608.
“Protein kinase Calpha-induced p115RhoGEF phosphorylation signals endothelial cytoskeletal rearrangement”. The Journal of Biological Chemistry 278 (31): 28793–8. (August 2003). doi:10.1074/jbc.M303900200. PMID 12754211.
“Centaurin-alpha(1) associates with and is phosphorylated by isoforms of protein kinase C”. Biochemical and Biophysical Research Communications 307 (3): 459–65. (August 2003). doi:10.1016/s0006-291x(03)01187-2. PMID 12893243.
“Protein kinase C alpha phosphorylates and negatively regulates diacylglycerol kinase zeta”. The Journal of Biological Chemistry 278 (41): 39542–7. (October 2003). doi:10.1074/jbc.M307153200. PMID 12890670.
“The small GTP-binding protein, Rhes, regulates signal transduction from G protein-coupled receptors”. Oncogene 23 (2): 559–68. (January 2004). doi:10.1038/sj.onc.1207161. PMID 14724584.
“The leucine-rich repeat protein SUR-8 enhances MAP kinase activation and forms a complex with Ras and Raf”. Genes & Development 14 (8): 895–900. (April 2000). doi:10.1101/gad.14.8.895. PMC 316541. PMID 10783161.
“Activation of phosphoinositide 3-kinase by interaction with Ras and by point mutation”. The EMBO Journal 15 (10): 2442–51. (May 1996). doi:10.1002/j.1460-2075.1996.tb00602.x. PMC 450176. PMID 8665852.
“The anti-apoptotic effect of Notch-1 requires p56lck-dependent, Akt/PKB-mediated signaling in T cells”. The Journal of Biological Chemistry 279 (4): 2937–44. (January 2004). doi:10.1074/jbc.M309924200. PMID 14583609.
“Phosphatidylinositol (PI) 3-kinase and PI 4-kinase binding to the CD4-p56lck complex: the p56lck SH3 domain binds to PI 3-kinase but not PI 4-kinase”. Molecular and Cellular Biology 13 (12): 7708–17. (December 1993). doi:10.1128/mcb.13.12.7708. PMC 364842. PMID 8246987.

pmc.ncbi.nlm.nih.gov

Rommel, Christian, ed (2010-01-01). “Oncogenic mutations of PIK3CA in human cancers”. Phosphoinositide 3-kinase in Health and Disease. Current Topics in Microbiology and Immunology. 347. Springer Berlin Heidelberg. pp. 21–41. doi:10.1007/82_2010_68. ISBN 9783642148156. PMC 3164550. PMID 20535651
“PIK3CA mutations in breast cancer: reconciling findings from preclinical and clinical data”. Breast Cancer Research 16 (1): 201. (January 2014). doi:10.1186/bcr3605. PMC 4054885. PMID 25192370.
“Aspirin use, tumor PIK3CA mutation, and colorectal-cancer survival”. The New England Journal of Medicine 367 (17): 1596–606. (October 2012). doi:10.1056/nejmoa1207756. PMC 3532946. PMID 23094721.
“Somatic Activating PIK3CA Mutations Cause Venous Malformation”. American Journal of Human Genetics 97 (6): 914–21. (December 2015). doi:10.1016/j.ajhg.2015.11.011. PMC 4678782. PMID 26637981.
“Lymphatic and other vascular malformative/overgrowth disorders are caused by somatic mutations in PIK3CA”. The Journal of Pediatrics 166 (4): 1048–54.e1–5. (April 2015). doi:10.1016/j.jpeds.2014.12.069. PMC 4498659. PMID 25681199.
“The leucine-rich repeat protein SUR-8 enhances MAP kinase activation and forms a complex with Ras and Raf”. Genes & Development 14 (8): 895–900. (April 2000). doi:10.1101/gad.14.8.895. PMC 316541. PMID 10783161.
“Activation of phosphoinositide 3-kinase by interaction with Ras and by point mutation”. The EMBO Journal 15 (10): 2442–51. (May 1996). doi:10.1002/j.1460-2075.1996.tb00602.x. PMC 450176. PMID 8665852.
“Phosphatidylinositol (PI) 3-kinase and PI 4-kinase binding to the CD4-p56lck complex: the p56lck SH3 domain binds to PI 3-kinase but not PI 4-kinase”. Molecular and Cellular Biology 13 (12): 7708–17. (December 1993). doi:10.1128/mcb.13.12.7708. PMC 364842. PMID 8246987.

ncbi.nlm.nih.gov

Human PubMed Reference:
Mouse PubMed Reference:
“Entrez Gene: PIK3CA”. 2023年9月15日閲覧。
Pagon, Roberta A., ed (1993-01-01). “PIK3CA-Related Overgrowth Spectrum”. PIK3CA-Related Segmental Overgrowth. University of Washington, Seattle. PMID 23946963

wikipedia.org (Global: low place; Japanese: low place)

en.wikipedia.org

GRCh38: Ensembl release 89: ENSG00000121879 - Ensembl, May 2017
GRCm38: Ensembl release 89: ENSMUSG00000027665 - Ensembl, May 2017

zenodo.org (Global: 621^st place; Japanese: 4,635^th place)

“Evaluation of PIK3CA mutation as a predictor of benefit from nonsteroidal anti-inflammatory drug therapy in colorectal cancer”. Journal of Clinical Oncology 31 (34): 4297–305. (December 2013). doi:10.1200/jco.2013.50.0322. PMID 24062397. https://zenodo.org/record/3439753. ^{[リンク切れ]}