Abl (gen)

С Википедије, слободне енциклопедије
ABL proto-onkogen 1, nereceptorska tirozinska kinaza
PDB prikaz baziran na 1ab2.
Dostupne strukture
1AB2​, 1ABL​, 1AWO​, 1BBZ​, 1JU5​, 1OPL​, 1ZZP​, 2ABL​, 2E2B​, 2F4J​, 2FO0​, 2G1T​, 2G2F​, 2G2H​, 2G2I​, 2GQG​, 2HIW​, 2HYY​, 2HZ0​, 2HZ4​, 2HZI​, 2O88​, 2V7A​, 3CS9​, 3EG0​, 3EG1​, 3EG2​, 3EG3​, 3EGU​, 3K2M​, 3PYY​, 3QRI​, 3QRJ​, 3QRK​, 3T04​, 3UE4​, 3UYO​, 4J9B​, 4J9C​, 4J9D​, 4J9E​, 4J9F​, 4J9G​, 4J9H​, 4J9I​, 4JJB​, 4JJC​, 4JJD​
Identifikatori
Simboli ABL1; ABL; JTK7; bcr/abl; c-ABL; c-ABL1; p150; v-abl
Vanjski ID OMIM: 189980 MGI: 87859 HomoloGene: 3783 GeneCards: ABL1 Gene
EC broj 2.7.10.2
Pregled RNK izražavanja
podaci
Ortolozi
Vrsta Čovek Miš
Entrez 25 11350
Ensembl ENSG00000097007 ENSMUSG00000026842
UniProt P00519 P00520
RefSeq (mRNA) NM_005157 NM_001112703
RefSeq (protein) NP_005148 NP_001106174
Lokacija (UCSC) Chr 9:
133.59 - 133.76 Mb		 Chr 2:
31.69 - 31.8 Mb
PubMed pretraga [1] [2]

Abelsonov mišji leukemijski viralni onkogen homolog 1 (ABL1) protein je koji je kod ljudi kodiran ABL1 genom (raniji simbol ABL) lociranim na hromozomu 9.[1] c-Abl se ponekad koristi za imenovanje verzije gena prisutnog u genomu sisara, dok se v-Abl odnosi na viralni gen.

Interakcije[уреди | уреди извор]

Abl gen formira interakcije sa:

Regulacija[уреди | уреди извор]

Postoje izvesni dokazi da je izražavanje Abl regulisano posredstvom mikroRNK miR-203.[50]

Vidi još[уреди | уреди извор]

Reference[уреди | уреди извор]

  1. ^ Szczylik C, Skorski T, Nicolaides NC, Manzella L, Malaguarnera L, Venturelli D, Gewirtz AM, Calabretta B (avgust 1991). „Selective inhibition of leukemia cell proliferation by BCR-ABL antisense oligodeoxynucleotides”. Science. 253 (5019): 562—5. PMID 1857987. doi:10.1126/science.1857987. 
  2. ^ Tani K; Sato Seiichi; Sukezane Taiko; Kojima Hiroshi; Hirose Hidenori; Hanafusa Hidesaburo; Shishido Tomoyuki (jun 2003). „Abl interactor 1 promotes tyrosine 296 phosphorylation of mammalian enabled (Mena) by c-Abl kinase”. J. Biol. Chem. 278 (24): 21685—92. PMID 12672821. doi:10.1074/jbc.M301447200. 
  3. ^ Biesova Z, Piccoli C, Wong WT (januar 1997). „Isolation and characterization of e3B1, an eps8 binding protein that regulates cell growth”. Oncogene. 14 (2): 233—41. PMID 9010225. doi:10.1038/sj.onc.1200822. 
  4. ^ Yamamoto A, Suzuki T, Sakaki Y (jun 2001). „Isolation of hNap1BP which interacts with human Nap1 (NCKAP1) whose expression is down-regulated in Alzheimer's disease”. Gene. 271 (2): 159—69. PMID 11418237. doi:10.1016/S0378-1119(01)00521-2. 
  5. ^ а б Cao C, Leng Y, Li C, Kufe D (april 2003). „Functional interaction between the c-Abl and Arg protein-tyrosine kinases in the oxidative stress response”. J. Biol. Chem. 278 (15): 12961—7. PMID 12569093. doi:10.1074/jbc.M300058200. 
  6. ^ Dai Z, Pendergast AM (novembar 1995). „Abi-2, a novel SH3-containing protein interacts with the c-Abl tyrosine kinase and modulates c-Abl transforming activity”. Genes Dev. 9 (21): 2569—82. PMID 7590236. doi:10.1101/gad.9.21.2569. 
  7. ^ а б Chen G, Yuan SS, Liu W, Xu Y, Trujillo K, Song B, Cong F, Goff SP, Wu Y, Arlinghaus R, Baltimore D, Gasser PJ, Park MS, Sung P, Lee EY (april 1999). „Radiation-induced assembly of Rad51 and Rad52 recombination complex requires ATM and c-Abl”. J. Biol. Chem. 274 (18): 12748—52. PMID 10212258. doi:10.1074/jbc.274.18.12748. 
  8. ^ Shafman T, Khanna KK, Kedar P, Spring K, Kozlov S, Yen T, Hobson K, Gatei M, Zhang N, Watters D, Egerton M, Shiloh Y, Kharbanda S, Kufe D, Lavin MF (maj 1997). „Interaction between ATM protein and c-Abl in response to DNA damage”. Nature. 387 (6632): 520—3. PMID 9168117. doi:10.1038/387520a0. 
  9. ^ а б Kishi S, Zhou XZ, Ziv Y, Khoo C, Hill DE, Shiloh Y, Lu KP (avgust 2001). „Telomeric protein Pin2/TRF1 as an important ATM target in response to double strand DNA breaks”. J. Biol. Chem. 276 (31): 29282—91. PMID 11375976. doi:10.1074/jbc.M011534200. 
  10. ^ Salgia R, Pisick E, Sattler M, Li JL, Uemura N, Wong WK, Burky SA, Hirai H, Chen LB, Griffin JD (oktobar 1996). „p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogene”. J. Biol. Chem. 271 (41): 25198—203. PMID 8810278. doi:10.1074/jbc.271.41.25198. 
  11. ^ Mayer BJ, Hirai H, Sakai R (mart 1995). „Evidence that SH2 domains promote processive phosphorylation by protein-tyrosine kinases”. Curr. Biol. 5 (3): 296—305. PMID 7780740. doi:10.1016/S0960-9822(95)00060-1. 
  12. ^ а б Puil L, Liu J, Gish G, Mbamalu G, Bowtell D, Pelicci PG, Arlinghaus R, Pawson T (februar 1994). „Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway”. EMBO J. 13 (4): 764—73. PMC 394874 Слободан приступ. PMID 8112292. 
  13. ^ Ling X; Ma Guozhen; Sun Tong; Liu Jiaxin; Arlinghaus Ralph B (januar 2003). „Bcr and Abl interaction: oncogenic activation of c-Abl by sequestering Bcr”. Cancer Res. 63 (2): 298—303. PMID 12543778. 
  14. ^ Pendergast AM, Muller AJ, Havlik MH, Maru Y, Witte ON (jul 1991). „BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner”. Cell. 66 (1): 161—71. PMID 1712671. doi:10.1016/0092-8674(91)90148-R. 
  15. ^ Foray N; Marot Didier; Randrianarison Voahangy; Venezia Nicole Dalla; Picard Didier; Perricaudet Michel; Favaudon Vincent; Jeggo Penny (jun 2002). „Constitutive Association of BRCA1 and c-Abl and Its ATM-Dependent Disruption after Irradiation”. Mol. Cell. Biol. 22 (12): 4020—32. PMC 133860 Слободан приступ. PMID 12024016. doi:10.1128/MCB.22.12.4020-4032.2002. 
  16. ^ Cao C; Leng Yumei; Kufe Donald (avgust 2003). „Catalase activity is regulated by c-Abl and Arg in the oxidative stress response”. J. Biol. Chem. 278 (32): 29667—75. PMID 12777400. doi:10.1074/jbc.M301292200. 
  17. ^ а б Miyoshi-Akiyama T, Aleman LM, Smith JM, Adler CE, Mayer BJ (jul 2001). „Regulation of Cbl phosphorylation by the Abl tyrosine kinase and the Nck SH2/SH3 adaptor”. Oncogene. 20 (30): 4058—69. PMID 11494134. doi:10.1038/sj.onc.1204528. 
  18. ^ а б Soubeyran P, Barac A, Szymkiewicz I, Dikic I (februar 2003). „Cbl-ArgBP2 complex mediates ubiquitination and degradation of c-Abl”. Biochem. J. 370 (Pt 1): 29—34. PMC 1223168 Слободан приступ. PMID 12475393. doi:10.1042/BJ20021539. 
  19. ^ а б в Ren R, Ye ZS, Baltimore D (april 1994). „Abl protein-tyrosine kinase selects the Crk adapter as a substrate using SH3-binding sites”. Genes Dev. 8 (7): 783—95. PMID 7926767. doi:10.1101/gad.8.7.783. 
  20. ^ Heaney C, Kolibaba K, Bhat A, Oda T, Ohno S, Fanning S, Druker BJ (januar 1997). „Direct binding of CRKL to BCR-ABL is not required for BCR-ABL transformation”. Blood. 89 (1): 297—306. PMID 8978305. 
  21. ^ Kyono WT, de Jong R, Park RK, Liu Y, Heisterkamp N, Groffen J, Durden DL (novembar 1998). „Differential interaction of Crkl with Cbl or C3G, Hef-1, and gamma subunit immunoreceptor tyrosine-based activation motif in signaling of myeloid high affinity Fc receptor for IgG (Fc gamma RI)”. J. Immunol. 161 (10): 5555—63. PMID 9820532. 
  22. ^ van Dijk TB; van Den Akker E; Amelsvoort M P; Mano H; Löwenberg B; von Lindern M (novembar 2000). „Stem cell factor induces phosphatidylinositol 3'-kinase-dependent Lyn/Tec/Dok-1 complex formation in hematopoietic cells”. Blood. 96 (10): 3406—13. PMID 11071635. 
  23. ^ Yamanashi Y, Baltimore D (januar 1997). „Identification of the Abl- and rasGAP-associated 62 kDa protein as a docking protein, Dok”. Cell. 88 (2): 205—11. PMID 9008161. doi:10.1016/S0092-8674(00)81841-3. 
  24. ^ Yu HH, Zisch AH, Dodelet VC, Pasquale EB (jul 2001). „Multiple signaling interactions of Abl and Arg kinases with the EphB2 receptor”. Oncogene. 20 (30): 3995—4006. PMID 11494128. doi:10.1038/sj.onc.1204524. 
  25. ^ Cao C; Leng Yumei; Huang Wei; Liu Xuan; Kufe Donald (oktobar 2003). „Glutathione peroxidase 1 is regulated by the c-Abl and Arg tyrosine kinases”. J. Biol. Chem. 278 (41): 39609—14. PMID 12893824. doi:10.1074/jbc.M305770200. 
  26. ^ Bai RY, Jahn T, Schrem S, Munzert G, Weidner KM, Wang JY, Duyster J (avgust 1998). „The SH2-containing adapter protein GRB10 interacts with BCR-ABL”. Oncogene. 17 (8): 941—8. PMID 9747873. doi:10.1038/sj.onc.1202024. 
  27. ^ Frantz JD, Giorgetti-Peraldi S, Ottinger EA, Shoelson SE (januar 1997). „Human GRB-IRbeta/GRB10. Splice variants of an insulin and growth factor receptor-binding protein with PH and SH2 domains”. J. Biol. Chem. 272 (5): 2659—67. PMID 9006901. doi:10.1074/jbc.272.5.2659. 
  28. ^ Kumar V, Sabatini D, Pandey P, Gingras AC, Majumder PK, Kumar M, Yuan ZM, Carmichael G, Weichselbaum R, Sonenberg N, Kufe D, Kharbanda S (april 2000). „Regulation of the rapamycin and FKBP-target 1/mammalian target of rapamycin and cap-dependent initiation of translation by the c-Abl protein-tyrosine kinase”. J. Biol. Chem. 275 (15): 10779—87. PMID 10753870. doi:10.1074/jbc.275.15.10779. 
  29. ^ Warmuth M, Bergmann M, Priess A, Häuslmann K, Emmerich B, Hallek M (decembar 1997). „The Src family kinase Hck interacts with Bcr-Abl by a kinase-independent mechanism and phosphorylates the Grb2-binding site of Bcr”. J. Biol. Chem. 272 (52): 33260—70. PMID 9407116. doi:10.1074/jbc.272.52.33260. 
  30. ^ Goldberg Z; Vogt Sionov Ronit; Berger Michael; Zwang Yaara; Perets Ruth; Van Etten Richard A; Oren Moshe; Taya Yoichi; Haupt Ygal (jul 2002). „Tyrosine phosphorylation of Mdm2 by c-Abl: implications for p53 regulation”. EMBO J. 21 (14): 3715—27. PMC 125401 Слободан приступ. PMID 12110584. doi:10.1093/emboj/cdf384. 
  31. ^ Minegishi M, Tachibana K, Sato T, Iwata S, Nojima Y, Morimoto C (oktobar 1996). „Structure and function of Cas-L, a 105-kD Crk-associated substrate- related protein that is involved in beta 1 integrin-mediated signaling in lymphocytes”. J. Exp. Med. 184 (4): 1365—75. PMC 2192828 Слободан приступ. PMID 8879209. doi:10.1084/jem.184.4.1365. 
  32. ^ Law SF, Estojak J, Wang B, Mysliwiec T, Kruh G, Golemis EA (jul 1996). „Human enhancer of filamentation 1, a novel p130cas-like docking protein, associates with focal adhesion kinase and induces pseudohyphal growth in Saccharomyces cerevisiae”. Mol. Cell. Biol. 16 (7): 3327—37. PMC 231327 Слободан приступ. PMID 8668148. 
  33. ^ Koch A, Mancini A, Stefan M, Niedenthal R, Niemann H, Tamura T (mart 2000). „Direct interaction of nerve growth factor receptor, TrkA, with non-receptor tyrosine kinase, c-Abl, through the activation loop”. FEBS Lett. 469 (1): 72—6. PMID 10708759. doi:10.1016/S0014-5793(00)01242-4. 
  34. ^ Yano H, Cong F, Birge RB, Goff SP, Chao MV (februar 2000). „Association of the Abl tyrosine kinase with the Trk nerve growth factor receptor”. J. Neurosci. Res. 59 (3): 356—64. PMID 10679771. doi:10.1002/(SICI)1097-4547(20000201)59:3<356::AID-JNR9>3.0.CO;2-G. 
  35. ^ Yuan ZM, Shioya H, Ishiko T, Sun X, Gu J, Huang YY, Lu H, Kharbanda S, Weichselbaum R, Kufe D (jun 1999). „p73 is regulated by tyrosine kinase c-Abl in the apoptotic response to DNA damage”. Nature. 399 (6738): 814—7. PMID 10391251. doi:10.1038/21704. 
  36. ^ Agami R, Blandino G, Oren M, Shaul Y (jun 1999). „Interaction of c-Abl and p73alpha and their collaboration to induce apoptosis”. Nature. 399 (6738): 809—13. PMID 10391250. doi:10.1038/21697. 
  37. ^ Wen ST, Van Etten RA (oktobar 1997). „The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity”. Genes Dev. 11 (19): 2456—67. PMC 316562 Слободан приступ. PMID 9334312. doi:10.1101/gad.11.19.2456. 
  38. ^ Roig J, Tuazon PT, Zipfel PA, Pendergast AM, Traugh JA (decembar 2000). „Functional interaction between c-Abl and the p21-activated protein kinase γ-PAK”. PNAS. 97 (26): 14346—51. PMC 18921 Слободан приступ. PMID 11121037. doi:10.1073/pnas.97.26.14346. 
  39. ^ Cong F, Spencer S, Côté JF, Wu Y, Tremblay ML, Lasky LA, Goff SP (decembar 2000). „Cytoskeletal protein PSTPIP1 directs the PEST-type protein tyrosine phosphatase to the c-Abl kinase to mediate Abl dephosphorylation”. Mol. Cell. 6 (6): 1413—23. PMID 11163214. doi:10.1016/S1097-2765(00)00138-6. 
  40. ^ Yoshida K; Komatsu Kiyoshi; Wang Hong-Gang; Kufe Donald (maj 2002). „c-Abl Tyrosine Kinase Regulates the Human Rad9 Checkpoint Protein in Response to DNA Damage”. Mol. Cell. Biol. 22 (10): 3292—300. PMC 133797 Слободан приступ. PMID 11971963. doi:10.1128/MCB.22.10.3292-3300.2002. 
  41. ^ Miyamura T, Nishimura J, Yufu Y, Nawata H (februar 1997). „Interaction of BCR-ABL with the retinoblastoma protein in Philadelphia chromosome-positive cell lines”. Int. J. Hematol. 65 (2): 115—21. PMID 9071815. doi:10.1016/S0925-5710(96)00539-7. 
  42. ^ Welch PJ, Wang JY (novembar 1993). „A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle”. Cell. 75 (4): 779—90. PMID 8242749. doi:10.1016/0092-8674(93)90497-E. 
  43. ^ Agami R, Shaul Y (april 1998). „The kinase activity of c-Abl but not v-Abl is potentiated by direct interaction with RFXI, a protein that binds the enhancers of several viruses and cell-cycle regulated genes”. Oncogene. 16 (14): 1779—88. PMID 9583676. doi:10.1038/sj.onc.1201708. 
  44. ^ Zhu J, Shore SK (decembar 1996). „c-ABL tyrosine kinase activity is regulated by association with a novel SH3-domain-binding protein”. Mol. Cell. Biol. 16 (12): 7054—62. PMC 231708 Слободан приступ. PMID 8943360. 
  45. ^ Wisniewski D, Strife A, Swendeman S, Erdjument-Bromage H, Geromanos S, Kavanaugh WM, Tempst P, Clarkson B (april 1999). „A novel SH2-containing phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase (SHIP2) is constitutively tyrosine phosphorylated and associated with src homologous and collagen gene (SHC) in chronic myelogenous leukemia progenitor cells”. Blood. 93 (8): 2707—20. PMID 10194451. 
  46. ^ Wang B, Golemis EA, Kruh GD (jul 1997). „ArgBP2, a multiple Src homology 3 domain-containing, Arg/Abl-interacting protein, is phosphorylated in v-Abl-transformed cells and localized in stress fibers and cardiocyte Z-disks”. J. Biol. Chem. 272 (28): 17542—50. PMID 9211900. doi:10.1074/jbc.272.28.17542. 
  47. ^ а б Ziemnicka-Kotula D, Xu J, Gu H, Potempska A, Kim KS, Jenkins EC, Trenkner E, Kotula L (maj 1998). „Identification of a candidate human spectrin Src homology 3 domain-binding protein suggests a general mechanism of association of tyrosine kinases with the spectrin-based membrane skeleton”. J. Biol. Chem. 273 (22): 13681—92. PMID 9593709. doi:10.1074/jbc.273.22.13681. 
  48. ^ Bassermann F, Jahn T, Miething C, Seipel P, Bai RY, Coutinho S, Tybulewicz VL, Peschel C, Duyster J (april 2002). „Association of Bcr-Abl with the proto-oncogene Vav is implicated in activation of the Rac-1 pathway”. J. Biol. Chem. 277 (14): 12437—45. PMID 11790798. doi:10.1074/jbc.M112397200. 
  49. ^ Rafalska I, Zhang Z, Benderska N, Wolff H, Hartmann AM, Brack-Werner R, Stamm S (avgust 2004). „The intranuclear localization and function of YT521-B is regulated by tyrosine phosphorylation”. Hum. Mol. Genet. 13 (15): 1535—49. PMID 15175272. doi:10.1093/hmg/ddh167. 
  50. ^ Bueno MJ, Pérez de Castro I, Gómez de Cedrón M, Santos J, Calin GA, Cigudosa JC, Croce CM, Fernández-Piqueras J, Malumbres M (jun 2008). „Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression”. Cancer Cell. 13 (6): 496—506. PMID 18538733. doi:10.1016/j.ccr.2008.04.018. 

Literatura[уреди | уреди извор]

Spoljašnje veze[уреди | уреди извор]

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