Onkogen

Onkogèn utawi proto onkogèn proto oncogènè protèin ingkang ngerangsang pembelahan sèl.^[1] Onkogèn (Cithakan:Oncogene) inggih punika gen ingkang termodifikasi saéngga ningkatakén keganasan ing sèl tumor. Onkogen limrahipun gadhah peran ing tahap wiwit ing pembentukan tumor. Onkogèn ningkataken sèl normal dados sèl tumor, ingkang pungkasan saged nyébapakén kankér. Riset ingkang ènggal inggih punika nunjuakén bawa RNA céndhak (small RNA) dawane kira-kira 21-25 nukelotida ingkang dipuntepang dados RNA mikro (miRNA) saged ngontrol onkogèn. Onkogen dipuntemuaken déning Francis Peyton Rous ing taun 1910.^[2] manawi ngamati tumor ing unggas ingkang saged dipuntransmisiken ing makluk sases amergi gadhah sel sarkoma ingkang ngandut retrovirus, ingkang lajengipun dipunsebat RSV (Inggris: Rous sarcoma virus).^[3]

Ing Taun 1976 Dr. John Michael Bishop lan Dr. Harold E. Varmus saking Universitas California San Francisco buktiaken manawi onkogen asalipun saking proto-onkogen ingkang ngalami karusakan. Proto-onkogen sampun kapanggih ingkang kathah organisme, kagolong manungsa ugi. Manawi ing pamanggihipun ingkang wigati punika , Dr. Bishop sahs Dr. Varmus angsal Penghargaan Nobel ing taun 1989.

Jinis

v-erbA inggih punika protéin onkogen asalipun saking proto-onkogen c-erbA tipe alfa yang wujud pencerap inti hormon T3/T4,^[4] dan asem retinoat,^[5] yang teraktivasi olèh avian erythroblastosis virus (AEV),^[6] yang ngakibatken leukimia ing pitik kaliyan ngambat diferensiasinipun sel progenitor eritrosit lan micu transformasi sarkoma.^[5]

Proto-onkogen

Proto-onkogen inggih punika gen normal ingkang saged dados onkogen mila ngalampahi mutasi, utawi mila ekspresinipun ningkataken. Proto-onkogen mengkode protéin ingkangg dipunbetahake sel kanggé regulasi pangerembagan lan dipunferensiasi. Proto-onkogen asring dipuntemuaken peran ing transduksi sinyal lan eksekusi sinyal mitogen, ingkang limrahipun dipunlampahi kaliyan produk protéin ingkang dipunkasilaken. sasampunipun dipunaktifaken, proto-onkogen utawi produk ingkang dipunkasilaken dados penginduksi tumor ingkang dipunsebat onkogen.

Aktivasi

Proto-onkogen saged dados onkogen kaliyan kedhik modifikasi ing fungsi aslinipun. Wonten kalih tipe pengaktifan:

kadadosan mutasi ing satu onkogen ingkang ngakibat owah-owahan ing struktur protéin, ingkang dipunsebatake kaliyan :

kenaikan aktivitas protéin (enzim)
icalipuna regulasi
kadadosan hibrid ing protéin nglampahi kerusakan kromosom ing pembelahan sel. Sampun dipunmangertosi bahwa kerusakan kromosom ingkang kadadosan ing wanci pembelahan sel ing sungsum balung belakang saged nimbulkan leukemia.

ningkataken konsèntrasi protéin, ingkang dipunsebataken kaliyan:

ningkataken èksprèsi protéin akibat kaluputan regulasi
ningkataken stabilitas protéin, ingkang damel kawontenan lan aktivitasipun ing salebeting sel dados langkung lami.
duplikasi gen, ingkang berakinate ningkatipun jumlah protéin ing sel.

Cathetan suku

↑ Campbell,Neil A,dkk."BIOLOGI Edisi Kedelapan Jilid 1".ISBN.Erlangga.Jakarta.(2008:404)
↑ "A transmissible avian neoplasm. (Sarcoma of the common fowl) by Peyton Rous, M.D., Experimental Medicine for Sept. 1, 1910, vol. 12, pp.696-705". Rous P. Dibukak ing 2010-09-18.
↑ Kufe, Donald W.; Pollock, Raphael E.; Weichselbaum, Ralph R.; Bast, Robert C., Jr.; Gansler, Ted S.; Holland, James F.; Frei III, Emil. (2003). Holland-Frei Cancer medicine. Dana-Farber Cancer Institute, Harvard Medical School Boston, Department of Surgical Oncology, University of Texas, MD Anderson Cancer Center, Department of Radiation and Cellular Oncology, University of Chicago Hospital, Chicago Tumor Institute, University of Chicago Chicago, University of Texas, MD Anderson Cancer Center, Houston, American Cancer Society, Derald H Ruttenberg Cancer Center, Mount Sinai School of Medicine New York (édhisi ka-6). Hamilton on BC Decker Inc.,. kc. Discovery and identification of oncogenes. ISBN 1-55009-213-8. Dibukak ing 2010-09-18.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
↑ "v-erbA overexpression is required to extinguish c-erbA function in erythroid cell differentiation and regulation of the erbA target gene CAII". Institute for Molecular Pathology; Disela C, Glineur C, Bugge T, Sap J, Stengl G, Dodgson J, Stunnenberg H, Beug H, Zenke M. Dibukak ing 2010-09-18.
↑ ^a ^b "[V-erbA oncogene, model of oncogenic activation of hormone receptor]". Laboratoire de Biologie Moléculaire et Cellulaire; Samarut J. Dibukak ing 2010-09-18.
↑ "The thyroid hormone receptor functions as a ligand-operated developmental switch between proliferation and differentiation of erythroid progenitors". Institute of Molecular Pathology (I.M.P.), Vienna Biocenter; Bauer A, Mikulits W, Anggara A, Stengl G, Brosch G, Beug H. Dibukak ing 2010-09-18.

[buku1-1] Campbell,Neil A,dkk."BIOLOGI Edisi Kedelapan Jilid 1".ISBN.Erlangga.Jakarta.(2008:404)

[2] "A transmissible avian neoplasm. (Sarcoma of the common fowl) by Peyton Rous, M.D., Experimental Medicine for Sept. 1, 1910, vol. 12, pp.696-705". Rous P. Dibukak ing 2010-09-18.

[3] Kufe, Donald W.; Pollock, Raphael E.; Weichselbaum, Ralph R.; Bast, Robert C., Jr.; Gansler, Ted S.; Holland, James F.; Frei III, Emil. (2003). Holland-Frei Cancer medicine. Dana-Farber Cancer Institute, Harvard Medical School Boston, Department of Surgical Oncology, University of Texas, MD Anderson Cancer Center, Department of Radiation and Cellular Oncology, University of Chicago Hospital, Chicago Tumor Institute, University of Chicago Chicago, University of Texas, MD Anderson Cancer Center, Houston, American Cancer Society, Derald H Ruttenberg Cancer Center, Mount Sinai School of Medicine New York (édhisi ka-6). Hamilton on BC Decker Inc.,. kc. Discovery and identification of oncogenes. ISBN 1-55009-213-8. Dibukak ing 2010-09-18.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)

[4] "v-erbA overexpression is required to extinguish c-erbA function in erythroid cell differentiation and regulation of the erbA target gene CAII". Institute for Molecular Pathology; Disela C, Glineur C, Bugge T, Sap J, Stengl G, Dodgson J, Stunnenberg H, Beug H, Zenke M. Dibukak ing 2010-09-18.

[PM1668630-5] "[V-erbA oncogene, model of oncogenic activation of hormone receptor]". Laboratoire de Biologie Moléculaire et Cellulaire; Samarut J. Dibukak ing 2010-09-18.

[6] "The thyroid hormone receptor functions as a ligand-operated developmental switch between proliferation and differentiation of erythroid progenitors". Institute of Molecular Pathology (I.M.P.), Vienna Biocenter; Bauer A, Mikulits W, Anggara A, Stengl G, Brosch G, Beug H. Dibukak ing 2010-09-18.

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