Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze
MARP protein family: A possible role in molecular mechanisms of tumorigenesis
Abstract
Familiju MARP (muscle ankyrin repeat proteins) čine tri strukturno slična proteina: CARP/Ankrd1, Ankrd2/Arpp i DARP/Ankrd23. Sva tri proteina poseduju ankirinske ponovke preko kojih ostvaruju protein-protein interakcije kao i signal za lokalizaciju u jedru. Članovi familije MARP imaju strukturnu i regulatornu funkciju i mogu biti lokalizovani i u jedru i u citoplazmi mišićne ćelije. Učestvuju u signalnoj transdukciji kao molekulski glasnici koji prenose informacije mehaničkog stresa sa sarkomere do jedra, gde učestvuju u regulaciji genske ekspresije. Nivo proteina CARP/Ankrd1 i Ankrd2/Arpp je izmenjen u mišićnim bolestima koje karakteriše atrofija mišića, kao što su Dišenova mišićna distrofija, kongenitalna miopatija i spinalna mišićna atrofija. Mutacije u genu za CARP/Ankrd1 su otkrivene u pacijenata sa dilatiranom i hipertrofičnom kardiomiopatijom. Promene u ekspresiji ovih proteina su takođe uočene u tumorima kao što su rabdomiosarkom, onkocitom bubrega i kancer ovarijuma. U cilju f...unkcionalne karakterizacije proteina familije MARP, pokazali smo da oba proteina interaguju sa supresorom tumora p53, a geni za CARP/Ankrd1 i Ankrd2/Arpp su pozitivno regulisani ovim transkripcionim faktorom. Rezultati su ukazali na moguću ulogu proteina CARP/Ankrd1 i Ankrd2/Arpp u molekularnim mehanizmima tumorogeneze, čime se otvara novo polje istraživanja ove familije proteina.
The MARP (muscle ankyrin repeat protein) family comprises three structurally similar proteins: CARP/Ankrd1, Ankrd2/Arpp and DARP/Ankrd23. They share four conserved copies of 33-residue ankyrin repeats and contain a nuclear localization signal, allowing the sorting of MARPs to the nucleus. They are found both in the nucleus and in the cytoplasm of skeletal and cardiac muscle cells, suggesting that MARPs shuttle within the cell enabling them to play a role in signal transduction in striated muscle. Expression of MARPs is altered under different pathological conditions. In skeletal muscle, CARP/Ankrd1 and Ankrd2/Arpp are up-regulated in muscle in patients suffering from Duchene muscular dystrophy, congenital myopathy and spinal muscular atrophy. Mutations in Ankrd1 gene (coding CARP/Ankrd1) were identified in dilated and hypertrophic cardiomyopathies. Altered expression of MARPs is also observed in rhabdomyosarcoma, renal oncocytoma and ovarian cancer. In order to functionally characteriz...e MARP family members CARP/Ankrd1 and Ankrd2/Arpp, we have found that both proteins interact with the tumor suppressor p53 both in vivo and in vitro and that p53 up-regulates their expression. Our results implicate the potential role of MARPs in molecular mechanisms relevant to tumor response and progression.
Keywords:
tumorogeneza / p53 / MARP / tumorigenesis / p53 / MARPsSource:
Journal of Medical Biochemistry, 2010, 29, 3, 157-164Publisher:
- Društvo medicinskih biohemičara Srbije, Beograd i Versita
Funding / projects:
- ICGEB, Italy [CRP/YUG-05-01]
- Strukturalni elementi genoma u modulaciji fenotipa (RS-MESTD-MPN2006-2010-143051)
DOI: 10.2478/v10011-010-0024-9
ISSN: 1452-8258
WoS: 000280477800005
Scopus: 2-s2.0-77955238689
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Institut za molekularnu genetiku i genetičko inženjerstvoTY - JOUR AU - Kojić, Snežana PY - 2010 UR - https://imagine.imgge.bg.ac.rs/handle/123456789/456 AB - Familiju MARP (muscle ankyrin repeat proteins) čine tri strukturno slična proteina: CARP/Ankrd1, Ankrd2/Arpp i DARP/Ankrd23. Sva tri proteina poseduju ankirinske ponovke preko kojih ostvaruju protein-protein interakcije kao i signal za lokalizaciju u jedru. Članovi familije MARP imaju strukturnu i regulatornu funkciju i mogu biti lokalizovani i u jedru i u citoplazmi mišićne ćelije. Učestvuju u signalnoj transdukciji kao molekulski glasnici koji prenose informacije mehaničkog stresa sa sarkomere do jedra, gde učestvuju u regulaciji genske ekspresije. Nivo proteina CARP/Ankrd1 i Ankrd2/Arpp je izmenjen u mišićnim bolestima koje karakteriše atrofija mišića, kao što su Dišenova mišićna distrofija, kongenitalna miopatija i spinalna mišićna atrofija. Mutacije u genu za CARP/Ankrd1 su otkrivene u pacijenata sa dilatiranom i hipertrofičnom kardiomiopatijom. Promene u ekspresiji ovih proteina su takođe uočene u tumorima kao što su rabdomiosarkom, onkocitom bubrega i kancer ovarijuma. U cilju funkcionalne karakterizacije proteina familije MARP, pokazali smo da oba proteina interaguju sa supresorom tumora p53, a geni za CARP/Ankrd1 i Ankrd2/Arpp su pozitivno regulisani ovim transkripcionim faktorom. Rezultati su ukazali na moguću ulogu proteina CARP/Ankrd1 i Ankrd2/Arpp u molekularnim mehanizmima tumorogeneze, čime se otvara novo polje istraživanja ove familije proteina. AB - The MARP (muscle ankyrin repeat protein) family comprises three structurally similar proteins: CARP/Ankrd1, Ankrd2/Arpp and DARP/Ankrd23. They share four conserved copies of 33-residue ankyrin repeats and contain a nuclear localization signal, allowing the sorting of MARPs to the nucleus. They are found both in the nucleus and in the cytoplasm of skeletal and cardiac muscle cells, suggesting that MARPs shuttle within the cell enabling them to play a role in signal transduction in striated muscle. Expression of MARPs is altered under different pathological conditions. In skeletal muscle, CARP/Ankrd1 and Ankrd2/Arpp are up-regulated in muscle in patients suffering from Duchene muscular dystrophy, congenital myopathy and spinal muscular atrophy. Mutations in Ankrd1 gene (coding CARP/Ankrd1) were identified in dilated and hypertrophic cardiomyopathies. Altered expression of MARPs is also observed in rhabdomyosarcoma, renal oncocytoma and ovarian cancer. In order to functionally characterize MARP family members CARP/Ankrd1 and Ankrd2/Arpp, we have found that both proteins interact with the tumor suppressor p53 both in vivo and in vitro and that p53 up-regulates their expression. Our results implicate the potential role of MARPs in molecular mechanisms relevant to tumor response and progression. PB - Društvo medicinskih biohemičara Srbije, Beograd i Versita T2 - Journal of Medical Biochemistry T1 - Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze T1 - MARP protein family: A possible role in molecular mechanisms of tumorigenesis EP - 164 IS - 3 SP - 157 VL - 29 DO - 10.2478/v10011-010-0024-9 ER -
@article{ author = "Kojić, Snežana", year = "2010", abstract = "Familiju MARP (muscle ankyrin repeat proteins) čine tri strukturno slična proteina: CARP/Ankrd1, Ankrd2/Arpp i DARP/Ankrd23. Sva tri proteina poseduju ankirinske ponovke preko kojih ostvaruju protein-protein interakcije kao i signal za lokalizaciju u jedru. Članovi familije MARP imaju strukturnu i regulatornu funkciju i mogu biti lokalizovani i u jedru i u citoplazmi mišićne ćelije. Učestvuju u signalnoj transdukciji kao molekulski glasnici koji prenose informacije mehaničkog stresa sa sarkomere do jedra, gde učestvuju u regulaciji genske ekspresije. Nivo proteina CARP/Ankrd1 i Ankrd2/Arpp je izmenjen u mišićnim bolestima koje karakteriše atrofija mišića, kao što su Dišenova mišićna distrofija, kongenitalna miopatija i spinalna mišićna atrofija. Mutacije u genu za CARP/Ankrd1 su otkrivene u pacijenata sa dilatiranom i hipertrofičnom kardiomiopatijom. Promene u ekspresiji ovih proteina su takođe uočene u tumorima kao što su rabdomiosarkom, onkocitom bubrega i kancer ovarijuma. U cilju funkcionalne karakterizacije proteina familije MARP, pokazali smo da oba proteina interaguju sa supresorom tumora p53, a geni za CARP/Ankrd1 i Ankrd2/Arpp su pozitivno regulisani ovim transkripcionim faktorom. Rezultati su ukazali na moguću ulogu proteina CARP/Ankrd1 i Ankrd2/Arpp u molekularnim mehanizmima tumorogeneze, čime se otvara novo polje istraživanja ove familije proteina., The MARP (muscle ankyrin repeat protein) family comprises three structurally similar proteins: CARP/Ankrd1, Ankrd2/Arpp and DARP/Ankrd23. They share four conserved copies of 33-residue ankyrin repeats and contain a nuclear localization signal, allowing the sorting of MARPs to the nucleus. They are found both in the nucleus and in the cytoplasm of skeletal and cardiac muscle cells, suggesting that MARPs shuttle within the cell enabling them to play a role in signal transduction in striated muscle. Expression of MARPs is altered under different pathological conditions. In skeletal muscle, CARP/Ankrd1 and Ankrd2/Arpp are up-regulated in muscle in patients suffering from Duchene muscular dystrophy, congenital myopathy and spinal muscular atrophy. Mutations in Ankrd1 gene (coding CARP/Ankrd1) were identified in dilated and hypertrophic cardiomyopathies. Altered expression of MARPs is also observed in rhabdomyosarcoma, renal oncocytoma and ovarian cancer. In order to functionally characterize MARP family members CARP/Ankrd1 and Ankrd2/Arpp, we have found that both proteins interact with the tumor suppressor p53 both in vivo and in vitro and that p53 up-regulates their expression. Our results implicate the potential role of MARPs in molecular mechanisms relevant to tumor response and progression.", publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita", journal = "Journal of Medical Biochemistry", title = "Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze, MARP protein family: A possible role in molecular mechanisms of tumorigenesis", pages = "164-157", number = "3", volume = "29", doi = "10.2478/v10011-010-0024-9" }
Kojić, S.. (2010). Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze. in Journal of Medical Biochemistry Društvo medicinskih biohemičara Srbije, Beograd i Versita., 29(3), 157-164. https://doi.org/10.2478/v10011-010-0024-9
Kojić S. Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze. in Journal of Medical Biochemistry. 2010;29(3):157-164. doi:10.2478/v10011-010-0024-9 .
Kojić, Snežana, "Proteini familije MARP - moguća uloga u molekularnim mehanizmima tumorogeneze" in Journal of Medical Biochemistry, 29, no. 3 (2010):157-164, https://doi.org/10.2478/v10011-010-0024-9 . .