Molekularni mehanizmi transdukcije hormonskih signala: Biološki markeri modifikacije i integracije signalnih puteva u fiziološkim i patofiziološkim stanjima

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Molekularni mehanizmi transdukcije hormonskih signala: Biološki markeri modifikacije i integracije signalnih puteva u fiziološkim i patofiziološkim stanjima (en)
Молекуларни механизми трансдукције хормонских сигнала: Биолошки маркери модификације и интеграције сигналних путева у физиолошким и патофизиолошким стањима (sr)
Molekularni mehanizmi transdukcije hormonskih signala: Biološki markeri modifikacije i integracije signalnih puteva u fiziološkim i patofiziološkim stanjima (sr_RS)
Authors

Publications

Uloga receptora aktiviranih proliferatorom peroksizoma u mehanizmu insulinske osetljivosti

Soskić, Sanja S.; Stanković, Aleksandra; Isenović, Esma R.; Alavantić, Dragan

(2010)

TY  - JOUR
AU  - Soskić, Sanja S.
AU  - Stanković, Aleksandra
AU  - Isenović, Esma R.
AU  - Alavantić, Dragan
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10329
AB  - Diabetes mellitus tipa 2 je hronično, progresivno, poligeno oboljenje koje karakteriše povećan nivo glukoze u cirkulaciji kao i drugi biohemijski poremećaji u organizmu. Nedavno otkriveni receptori aktivirani proliferatorom peroksizoma su transkripcioni faktori koji pripadaju superfamiliji nukleusnih receptora. Dva člana ove familije su receptori aktivirani proliferatorom peroksizoma alfa i gama koji predstavljaju nove gene kandidate za nastanak dijabetesa tipa 2 i metaboličkog sindroma (okarakterisanog kao predijabetesno stanje). Od velikog je značaja fiziološka uloga receptora aktiviranih proliferatorom peroksizoma gama kako u metabolizmu lipida i glukoze tako i u mehanizmu insulinske osetljivosti kome treba dati jedno od centralnih mesta u terapiji dijabetesa tipa 2.
AB  - Type 2 diabetes mellitus is a chronic, progressive, polygenic disease which is characterised by increased glucose levels in circulation and also by many other biochemical disturbances in diabetic patients. Recently discovered, peroxisomal proliferator-activated receptors are transcription factors and members of superfamily of nuclear receptors. Two members of this family peroxisomal proliferator-activated receptors alpha and gamma are novel candidate genes for the onset of type 2 diabetes and metabolic syndrome which is characterised as prediabetic condition. It is of great importance to understand physiological role of peroxisomal proliferator-activated receptors gamma as in lipid and glucose metabolism as in a mechanism of insulin sensitivity which is to be given one of the major role in therapy of type 2 diabetes.
T2  - Materia medica
T1  - Uloga receptora aktiviranih proliferatorom peroksizoma u mehanizmu insulinske osetljivosti
T1  - Role of peroxisomal proliferators: Activated receptors in mechanism of insulin sensitivity
VL  - 26
IS  - 1
SP  - 25
EP  - 31
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10329
ER  - 
@article{
author = "Soskić, Sanja S. and Stanković, Aleksandra and Isenović, Esma R. and Alavantić, Dragan",
year = "2010",
abstract = "Diabetes mellitus tipa 2 je hronično, progresivno, poligeno oboljenje koje karakteriše povećan nivo glukoze u cirkulaciji kao i drugi biohemijski poremećaji u organizmu. Nedavno otkriveni receptori aktivirani proliferatorom peroksizoma su transkripcioni faktori koji pripadaju superfamiliji nukleusnih receptora. Dva člana ove familije su receptori aktivirani proliferatorom peroksizoma alfa i gama koji predstavljaju nove gene kandidate za nastanak dijabetesa tipa 2 i metaboličkog sindroma (okarakterisanog kao predijabetesno stanje). Od velikog je značaja fiziološka uloga receptora aktiviranih proliferatorom peroksizoma gama kako u metabolizmu lipida i glukoze tako i u mehanizmu insulinske osetljivosti kome treba dati jedno od centralnih mesta u terapiji dijabetesa tipa 2., Type 2 diabetes mellitus is a chronic, progressive, polygenic disease which is characterised by increased glucose levels in circulation and also by many other biochemical disturbances in diabetic patients. Recently discovered, peroxisomal proliferator-activated receptors are transcription factors and members of superfamily of nuclear receptors. Two members of this family peroxisomal proliferator-activated receptors alpha and gamma are novel candidate genes for the onset of type 2 diabetes and metabolic syndrome which is characterised as prediabetic condition. It is of great importance to understand physiological role of peroxisomal proliferator-activated receptors gamma as in lipid and glucose metabolism as in a mechanism of insulin sensitivity which is to be given one of the major role in therapy of type 2 diabetes.",
journal = "Materia medica",
title = "Uloga receptora aktiviranih proliferatorom peroksizoma u mehanizmu insulinske osetljivosti, Role of peroxisomal proliferators: Activated receptors in mechanism of insulin sensitivity",
volume = "26",
number = "1",
pages = "25-31",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10329"
}
Soskić, S. S., Stanković, A., Isenović, E. R.,& Alavantić, D.. (2010). Uloga receptora aktiviranih proliferatorom peroksizoma u mehanizmu insulinske osetljivosti. in Materia medica, 26(1), 25-31.
https://hdl.handle.net/21.15107/rcub_vinar_10329
Soskić SS, Stanković A, Isenović ER, Alavantić D. Uloga receptora aktiviranih proliferatorom peroksizoma u mehanizmu insulinske osetljivosti. in Materia medica. 2010;26(1):25-31.
https://hdl.handle.net/21.15107/rcub_vinar_10329 .
Soskić, Sanja S., Stanković, Aleksandra, Isenović, Esma R., Alavantić, Dragan, "Uloga receptora aktiviranih proliferatorom peroksizoma u mehanizmu insulinske osetljivosti" in Materia medica, 26, no. 1 (2010):25-31,
https://hdl.handle.net/21.15107/rcub_vinar_10329 .

Uloga azot monoksida (NO) u gastrointestinalnom traktu (GIT)

Tepavčević, Snežana; Milovanović, Slobodan R.; Isenović, Esma R.

(2007)

TY  - JOUR
AU  - Tepavčević, Snežana
AU  - Milovanović, Slobodan R.
AU  - Isenović, Esma R.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10332
AB  - NO je veoma bitan inhibitorni neurotransmiter u GIT-u koji se oslobađa iz neadrenergičkih i neholinergičkih neurona. NO deluje kao unutar i ekstraćelijski signalni molekul u vaskularnim i glatkim mišićnim ćelijama GIT-a, i važan je medijator u brojnim fiziološkim i patofiziološkim stanjima. NO se sintetiše iz L-arginina pod dejstvom enzima azot monoksid sintetaze (NOS). NOS je lokalizovana u nitrergičkim neuronima u GIT-u, ali može se sintetisati i u drugim ćelijskim tipovima, kao što su glatke mišićne ćelije. Najšire prihvaćeno delovanje NO-a u crevu je relaksacija glatkih mišića putem aktivacije solubilne forme guanilil ciklaze i akumulacije cikličnog guanozin monofosfata (cGMP). U glatkim mišićima GIT-a, NO i donori NO izazivaju različite efekte: kontrakciju, relaksaciju praćenu kontrakcijom i kontrakciju praćenu relaksacijom, što zavisi od tipa NO donora, tkiva i vrste. Ekscitatorni efekt NO-a obuhvata holinergičke motorne neurone. Višestruko delovanje NO-a sugeriše da se manipulacijom NO sistema može uticati na enteričke motorne reflekse, kao i na peristaltiku tankog creva. Visoke koncentracije NO-a mogu oštetiti intestinalne epitelne ćelije, za šta je odgovoran cGMP. Odsustvo nitrergičke inervacije je pokazano u gastrointestinalnim tkivima pacijenata sa različitim bolestima, kao što su Ahalazija i Hirschsprungsova bolest.
AB  - NO is a very important inhibitory neurotransmitter in the GIT, released from non-adrenergic non-cholinergic neurons. NO acts as an intra- and extracellular signalling molecule in vascular and smooth muscle GIT cells and it is an important mediator in numerous physiological and pathophysiological conditions. NO is synthesized from L-arginine by the action of NO synthase (NOS) that is present in nitrergic neurons of GIT. NO could be also synthesized in other cell types such as smooth muscle cells. The most widely reported action of NO in the gut is relaxation of smooth muscle through activation of the soluble guanylate cyclase and the accumulation of the cyclic guanosine 3’, 5’-monophosphate (cGMP). In GIT smooth muscle cells, NO and NO donors evoke different responses including contractile effects, relaxations followed by contractions or contractions followed by relaxations, which depends on the type of NO donor, tissue and species. The excitatory effect of NO involves cholinergic motor neurons. Multiple actions of NO suggest that manipulation of the NO system may influence enteric motor reflexes and peristalsis of small intestine. Large amounts of NO can damage the intestine epithelial cells, and cGMP is responsible for this damage. Deficiency of nitrergic innervations has been shown in gastrointestinal tissues of patients with various diseases such as are Achalasia and Hirschsprung’s disease.
T2  - Timočki medicinski glasnik
T1  - Uloga azot monoksida (NO) u gastrointestinalnom traktu (GIT)
T1  - The role of nitric oxide (NO) in gastrointestinal tract (GIT)
VL  - 32
IS  - 1
SP  - 46
EP  - 51
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10332
ER  - 
@article{
author = "Tepavčević, Snežana and Milovanović, Slobodan R. and Isenović, Esma R.",
year = "2007",
abstract = "NO je veoma bitan inhibitorni neurotransmiter u GIT-u koji se oslobađa iz neadrenergičkih i neholinergičkih neurona. NO deluje kao unutar i ekstraćelijski signalni molekul u vaskularnim i glatkim mišićnim ćelijama GIT-a, i važan je medijator u brojnim fiziološkim i patofiziološkim stanjima. NO se sintetiše iz L-arginina pod dejstvom enzima azot monoksid sintetaze (NOS). NOS je lokalizovana u nitrergičkim neuronima u GIT-u, ali može se sintetisati i u drugim ćelijskim tipovima, kao što su glatke mišićne ćelije. Najšire prihvaćeno delovanje NO-a u crevu je relaksacija glatkih mišića putem aktivacije solubilne forme guanilil ciklaze i akumulacije cikličnog guanozin monofosfata (cGMP). U glatkim mišićima GIT-a, NO i donori NO izazivaju različite efekte: kontrakciju, relaksaciju praćenu kontrakcijom i kontrakciju praćenu relaksacijom, što zavisi od tipa NO donora, tkiva i vrste. Ekscitatorni efekt NO-a obuhvata holinergičke motorne neurone. Višestruko delovanje NO-a sugeriše da se manipulacijom NO sistema može uticati na enteričke motorne reflekse, kao i na peristaltiku tankog creva. Visoke koncentracije NO-a mogu oštetiti intestinalne epitelne ćelije, za šta je odgovoran cGMP. Odsustvo nitrergičke inervacije je pokazano u gastrointestinalnim tkivima pacijenata sa različitim bolestima, kao što su Ahalazija i Hirschsprungsova bolest., NO is a very important inhibitory neurotransmitter in the GIT, released from non-adrenergic non-cholinergic neurons. NO acts as an intra- and extracellular signalling molecule in vascular and smooth muscle GIT cells and it is an important mediator in numerous physiological and pathophysiological conditions. NO is synthesized from L-arginine by the action of NO synthase (NOS) that is present in nitrergic neurons of GIT. NO could be also synthesized in other cell types such as smooth muscle cells. The most widely reported action of NO in the gut is relaxation of smooth muscle through activation of the soluble guanylate cyclase and the accumulation of the cyclic guanosine 3’, 5’-monophosphate (cGMP). In GIT smooth muscle cells, NO and NO donors evoke different responses including contractile effects, relaxations followed by contractions or contractions followed by relaxations, which depends on the type of NO donor, tissue and species. The excitatory effect of NO involves cholinergic motor neurons. Multiple actions of NO suggest that manipulation of the NO system may influence enteric motor reflexes and peristalsis of small intestine. Large amounts of NO can damage the intestine epithelial cells, and cGMP is responsible for this damage. Deficiency of nitrergic innervations has been shown in gastrointestinal tissues of patients with various diseases such as are Achalasia and Hirschsprung’s disease.",
journal = "Timočki medicinski glasnik",
title = "Uloga azot monoksida (NO) u gastrointestinalnom traktu (GIT), The role of nitric oxide (NO) in gastrointestinal tract (GIT)",
volume = "32",
number = "1",
pages = "46-51",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10332"
}
Tepavčević, S., Milovanović, S. R.,& Isenović, E. R.. (2007). Uloga azot monoksida (NO) u gastrointestinalnom traktu (GIT). in Timočki medicinski glasnik, 32(1), 46-51.
https://hdl.handle.net/21.15107/rcub_vinar_10332
Tepavčević S, Milovanović SR, Isenović ER. Uloga azot monoksida (NO) u gastrointestinalnom traktu (GIT). in Timočki medicinski glasnik. 2007;32(1):46-51.
https://hdl.handle.net/21.15107/rcub_vinar_10332 .
Tepavčević, Snežana, Milovanović, Slobodan R., Isenović, Esma R., "Uloga azot monoksida (NO) u gastrointestinalnom traktu (GIT)" in Timočki medicinski glasnik, 32, no. 1 (2007):46-51,
https://hdl.handle.net/21.15107/rcub_vinar_10332 .

Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor

Žakula, Zorica; Isenović, Esma R.; Stojiljković, Mojca D.; Tepavčević, Snežana; Ribarac-Stepić, Nevena B.

(2007)

TY  - JOUR
AU  - Žakula, Zorica
AU  - Isenović, Esma R.
AU  - Stojiljković, Mojca D.
AU  - Tepavčević, Snežana
AU  - Ribarac-Stepić, Nevena B.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3412
AB  - The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.
T2  - Archives of Biological Sciences
T1  - Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor
VL  - 59
IS  - 2
SP  - 105
EP  - 112
DO  - 10.2298/ABS0702105Z
ER  - 
@article{
author = "Žakula, Zorica and Isenović, Esma R. and Stojiljković, Mojca D. and Tepavčević, Snežana and Ribarac-Stepić, Nevena B.",
year = "2007",
abstract = "The aim of this study was to examine the effects of estradiol (E2) on activity of RNA polymerase I and RNA polymerase II in uterine nuclei of ovariectomized (OVX) female rats. The obtained results show that estrogen-receptor (E-R) complexes in 30 min induced an increase of polymerase II activity. A second increase of polymerase II activity was observed after 3 h-incubation of nuclei with the E-R complex formed in the cytosol fraction. However, activity of polymerase I was increased 2 h after the start of incubation, with highest activity detected at 3 h in nuclei incubated with E-R complexes. On the contrary, no stimulatory effect on either polymerase I or polymerase II activity was observed in nuclei incubated with E2 alone. These results indicate that E2 stimulates the cytosolic estrogen receptor (ER), which in turn causes uterotrophic responses in OVX rats. In addition, they suggest that in order to provoke uterotrophic responses E-R complexes formed in the cytosol need to be retained in the nucleus for a longer period of time.",
journal = "Archives of Biological Sciences",
title = "Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor",
volume = "59",
number = "2",
pages = "105-112",
doi = "10.2298/ABS0702105Z"
}
Žakula, Z., Isenović, E. R., Stojiljković, M. D., Tepavčević, S.,& Ribarac-Stepić, N. B.. (2007). Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor. in Archives of Biological Sciences, 59(2), 105-112.
https://doi.org/10.2298/ABS0702105Z
Žakula Z, Isenović ER, Stojiljković MD, Tepavčević S, Ribarac-Stepić NB. Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor. in Archives of Biological Sciences. 2007;59(2):105-112.
doi:10.2298/ABS0702105Z .
Žakula, Zorica, Isenović, Esma R., Stojiljković, Mojca D., Tepavčević, Snežana, Ribarac-Stepić, Nevena B., "Estrogen-induced modification of uterine RNA polymerase activity depends on localization of the estrogen receptor" in Archives of Biological Sciences, 59, no. 2 (2007):105-112,
https://doi.org/10.2298/ABS0702105Z . .

Production and characterization of monoclonal antibodies specific for pseudorabies virus

Marković, Ljiljana; Ašanin, Ružica; Sonja, Radojicic; Isenović, Esma R.

(2007)

TY  - JOUR
AU  - Marković, Ljiljana
AU  - Ašanin, Ružica
AU  - Sonja, Radojicic
AU  - Isenović, Esma R.
PY  - 2007
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3337
AB  - Monoclonal antibodies (MAbs) against Pseudorabies virus (PrV) were obtained by the fusion of P3x-Ag8.653 myeloma and spleen cells from immunized BALB/c mice with a suspension of Pseudorabies (PrV) virus strains: MAVE (Morbus Aujeszky virus Ercegovac) and NS 257 (Novosadski virus strain). A total of 95 antibody-secreting hybridoma cells against the virus strain (MAVE and NS 257) of Pseudorabies virus have been isolated. Ten of these monoclonal antibodies were found by ELISA (Enzyme-linked immunosorbent assay) to react specifically with both virus strains. MAbs for VAM 2.1, VAM 4.1, VAM 5.1 and VAM 6.1 were purified by chromatography on protein G Sepharose 4FF and they have been shown to have a strong reactivity in the ELISA test. All MAbs were characterized by electrophoresis SDS-PAGE and electrophoresis Western-blot immunoassay, MAbs VAM 2.1, VAM 4.1, VAM 5.1 and VAM 6.1 in hybridoma culture supernatants and ascites fluid were quantified using a dot-blot immunobinding assay. The VAM 2.1 MAb was found to be more specific in the reaction with viruses of both strains. The glycoprotein of 40 kD molecular weight was found on the surface of virus strain MAVE. Results showed that the produced and characterized MAbs against PrV strains can be used for the detection of Aujeszkys disease.
AB  - Monoklonska antitela (MAbs) specifična za Pseudorabies virus (PrV) dobijena su fuzijom ćelija mijelocita P3x-Ag8.653 i splenocita miševa BALB/c koji su imunizovani suspenzijama sojeva MAVE (Morbus Aujeszk'y virus Ercegovac) i NS 257 (soj 257 Novi Sad). U 95 uzoraka supernatanata hibridnih ćelija primenom ELISA metode ispitivano je prisustvo antitela specifičnih za sojeve virusa (MAVE i NS 257). Navedenom metodom otkriveno je deset monoklonskih antitela koja su specifično reagovala sa oba soja virusa. Izdvojena četiri monoklonska antitela označena kao VAM2.1, VAM4.1, VAM5.1 i VAM 6.1, radi dalje analize, prečišćena su metodom hromatografije na koloni protein G Sepharosa 4FF, a zatim ponovo ispitana ELISA metodom. Karakterizacija izdvojenih MAbs za navedene viruse urađena je metodama elektroforeze SDS-PAGE i Westernblott. Dot-blott metodom iz supernatanata hibridnih ćelija i ascitne tečnosti kvantifikovana su monoklonska antitela VAM 2.1, VAM 4.1, VAM 5.1 i VAM 6.1. Monoklonsko antitelo VAM 2.1 pokazalo je visok nivo aktivnosti u reakciji sa oba soja virusa. Analizom proteinskog profila virusnog omotača soja MAVE detektovan je glikoprotein molekulske mase 40 kD. Ova ispitivanja su ukazala da monoklonska antitela specifična za sojeve PrV mogu da se primene u otkrivanju Aujeskijeve bolesti.
T2  - Acta Veterinaria, Beograd
T1  - Production and characterization of monoclonal antibodies specific for pseudorabies virus
T1  - Dobijanje i karakterizacija monoklonskih antitela specifičnih za Pseudorabies virus
VL  - 57
IS  - 5-6
SP  - 441
EP  - 451
DO  - 10.2298/AVB0706441M
ER  - 
@article{
author = "Marković, Ljiljana and Ašanin, Ružica and Sonja, Radojicic and Isenović, Esma R.",
year = "2007",
abstract = "Monoclonal antibodies (MAbs) against Pseudorabies virus (PrV) were obtained by the fusion of P3x-Ag8.653 myeloma and spleen cells from immunized BALB/c mice with a suspension of Pseudorabies (PrV) virus strains: MAVE (Morbus Aujeszky virus Ercegovac) and NS 257 (Novosadski virus strain). A total of 95 antibody-secreting hybridoma cells against the virus strain (MAVE and NS 257) of Pseudorabies virus have been isolated. Ten of these monoclonal antibodies were found by ELISA (Enzyme-linked immunosorbent assay) to react specifically with both virus strains. MAbs for VAM 2.1, VAM 4.1, VAM 5.1 and VAM 6.1 were purified by chromatography on protein G Sepharose 4FF and they have been shown to have a strong reactivity in the ELISA test. All MAbs were characterized by electrophoresis SDS-PAGE and electrophoresis Western-blot immunoassay, MAbs VAM 2.1, VAM 4.1, VAM 5.1 and VAM 6.1 in hybridoma culture supernatants and ascites fluid were quantified using a dot-blot immunobinding assay. The VAM 2.1 MAb was found to be more specific in the reaction with viruses of both strains. The glycoprotein of 40 kD molecular weight was found on the surface of virus strain MAVE. Results showed that the produced and characterized MAbs against PrV strains can be used for the detection of Aujeszkys disease., Monoklonska antitela (MAbs) specifična za Pseudorabies virus (PrV) dobijena su fuzijom ćelija mijelocita P3x-Ag8.653 i splenocita miševa BALB/c koji su imunizovani suspenzijama sojeva MAVE (Morbus Aujeszk'y virus Ercegovac) i NS 257 (soj 257 Novi Sad). U 95 uzoraka supernatanata hibridnih ćelija primenom ELISA metode ispitivano je prisustvo antitela specifičnih za sojeve virusa (MAVE i NS 257). Navedenom metodom otkriveno je deset monoklonskih antitela koja su specifično reagovala sa oba soja virusa. Izdvojena četiri monoklonska antitela označena kao VAM2.1, VAM4.1, VAM5.1 i VAM 6.1, radi dalje analize, prečišćena su metodom hromatografije na koloni protein G Sepharosa 4FF, a zatim ponovo ispitana ELISA metodom. Karakterizacija izdvojenih MAbs za navedene viruse urađena je metodama elektroforeze SDS-PAGE i Westernblott. Dot-blott metodom iz supernatanata hibridnih ćelija i ascitne tečnosti kvantifikovana su monoklonska antitela VAM 2.1, VAM 4.1, VAM 5.1 i VAM 6.1. Monoklonsko antitelo VAM 2.1 pokazalo je visok nivo aktivnosti u reakciji sa oba soja virusa. Analizom proteinskog profila virusnog omotača soja MAVE detektovan je glikoprotein molekulske mase 40 kD. Ova ispitivanja su ukazala da monoklonska antitela specifična za sojeve PrV mogu da se primene u otkrivanju Aujeskijeve bolesti.",
journal = "Acta Veterinaria, Beograd",
title = "Production and characterization of monoclonal antibodies specific for pseudorabies virus, Dobijanje i karakterizacija monoklonskih antitela specifičnih za Pseudorabies virus",
volume = "57",
number = "5-6",
pages = "441-451",
doi = "10.2298/AVB0706441M"
}
Marković, L., Ašanin, R., Sonja, R.,& Isenović, E. R.. (2007). Production and characterization of monoclonal antibodies specific for pseudorabies virus. in Acta Veterinaria, Beograd, 57(5-6), 441-451.
https://doi.org/10.2298/AVB0706441M
Marković L, Ašanin R, Sonja R, Isenović ER. Production and characterization of monoclonal antibodies specific for pseudorabies virus. in Acta Veterinaria, Beograd. 2007;57(5-6):441-451.
doi:10.2298/AVB0706441M .
Marković, Ljiljana, Ašanin, Ružica, Sonja, Radojicic, Isenović, Esma R., "Production and characterization of monoclonal antibodies specific for pseudorabies virus" in Acta Veterinaria, Beograd, 57, no. 5-6 (2007):441-451,
https://doi.org/10.2298/AVB0706441M . .

Insulin signaling pathway in skeletal muscles

Sudar, Emina; Velebit, Jelena; Isenović, Esma R.

(2006)

TY  - JOUR
AU  - Sudar, Emina
AU  - Velebit, Jelena
AU  - Isenović, Esma R.
PY  - 2006
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10334
AB  - Insulin (INS), the hormone of endocrine pancreas, is one of the most important vertebrate proteins. Increased circulating levels of glucose (Glu) stimulate pancreatic β cells to secrete INS by exocytosis. Insulin receptor (IR) belongs to the group of membrane receptors with tyrosine kinase activity. Skeletal muscles (SM) account for about 85% of total Glu disposal under INS stimulated conditions where it is incorporated and stored as glycogen. Glu entry into cells is a process that requires the involvement of a carrier protein in order to facilitate the movement of Glu across the plasma membrane of a cell and they are identified as glucose transporters (GLUT). In SMs, GLUT1 and GLUT4 are the primary GLUTs expressed. In SMs, INS stimulated Glu disposal is mediated via translocation of GLUT4 from intracellular storage site to the plasma membrane and GLUT1 primary mediates basal, rather than INS mediated Glu uptake. Impairment of the mechanisms responsible for this translocation leads to INS resistance. Peripheral INS resistance is a key factor in the pathogenesis of type 2 Diabetes Mellitus (DMT2) and involves defects in Glu transport system in adipocytes and SM. SM is the principal site of Glu uptake under INS stimulated conditions and INS resistance in SM has been identified as the most important site for INS resistance in DMT2 and may result from a defect at the level of Glu transport, Glu phosphorylation or glycogen synthesis. Glu transport is one of the first steps in INS stimulated Glu uptake in SM and it is a rate limiting factor in the whole Glu metabolism.
AB  - Insulin (INS) je hormon endokrinog pankreasa i jedan je od najznačajnijih proteina kičmenjaka. Povećana koncentracija glukoze (Glu) u krvi stimuliše β ćelije pankreasa i dovodi do sekrecije INS egzocitozom. Receptor za insulin (IR) pripada grupi membranskih receptora koji poseduju tirozin kinaznu aktivnost. Skeletni mišići (SM) preuzimaju oko 85% ukupne Glu pri insulinskoj stimulaciji i Glu se u njih inkorporira i skladišti u vidu glikogena. Glu u ćelije ulazi uz pomoć proteina nosača koji olakšavaju transport Glu kroz ćelijsku membranu i identifikovani su kao glukozni transporteri (GLUT). U ćelijama SM, lokalizovani su GLUT1 i GLUT4. INS stimulisano preuzimanje Glu u mišićnim ćelijama posredovano je translokacijom GLUT4 na površinu ćelijske membrane, dok GLUT1 posreduje u preuzimanju Glu u mišićne ćelije pri bazalnim uslovima. Poremećaji u mehanizmima koji su odgovorni za ovu translokaciju vode insulinskoj rezistenciji. Periferna insulinska resistencija koja uključuje poremećaje transporta Glu u adipocitima i SM, ključni je faktor u patogenezi Diabetesa Mellitusa tipa 2 (DMT2). S obzirom na to da SM preuzimaju najveći deo ukupne Glu, insulinska rezistencija u SM od velikog je značaja za razvoj DMT2 i može se javiti na tri nivoa: na nivou transporta Glu, fosforilacije Glu i na nivou sinteze glikogena. Transport Glu je osnovni korak u preuzimanju Glu u SM pri insulinskoj stimulaciji i ograničavajući je faktor za celokupan metabolizam Glu u organizmu.
T2  - Timočki medicinski glasnik
T1  - Insulin signaling pathway in skeletal muscles
T1  - Signalni put insulina u ćelijama skeletnih mišića
VL  - 31
IS  - 4
SP  - 180
EP  - 185
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10334
ER  - 
@article{
author = "Sudar, Emina and Velebit, Jelena and Isenović, Esma R.",
year = "2006",
abstract = "Insulin (INS), the hormone of endocrine pancreas, is one of the most important vertebrate proteins. Increased circulating levels of glucose (Glu) stimulate pancreatic β cells to secrete INS by exocytosis. Insulin receptor (IR) belongs to the group of membrane receptors with tyrosine kinase activity. Skeletal muscles (SM) account for about 85% of total Glu disposal under INS stimulated conditions where it is incorporated and stored as glycogen. Glu entry into cells is a process that requires the involvement of a carrier protein in order to facilitate the movement of Glu across the plasma membrane of a cell and they are identified as glucose transporters (GLUT). In SMs, GLUT1 and GLUT4 are the primary GLUTs expressed. In SMs, INS stimulated Glu disposal is mediated via translocation of GLUT4 from intracellular storage site to the plasma membrane and GLUT1 primary mediates basal, rather than INS mediated Glu uptake. Impairment of the mechanisms responsible for this translocation leads to INS resistance. Peripheral INS resistance is a key factor in the pathogenesis of type 2 Diabetes Mellitus (DMT2) and involves defects in Glu transport system in adipocytes and SM. SM is the principal site of Glu uptake under INS stimulated conditions and INS resistance in SM has been identified as the most important site for INS resistance in DMT2 and may result from a defect at the level of Glu transport, Glu phosphorylation or glycogen synthesis. Glu transport is one of the first steps in INS stimulated Glu uptake in SM and it is a rate limiting factor in the whole Glu metabolism., Insulin (INS) je hormon endokrinog pankreasa i jedan je od najznačajnijih proteina kičmenjaka. Povećana koncentracija glukoze (Glu) u krvi stimuliše β ćelije pankreasa i dovodi do sekrecije INS egzocitozom. Receptor za insulin (IR) pripada grupi membranskih receptora koji poseduju tirozin kinaznu aktivnost. Skeletni mišići (SM) preuzimaju oko 85% ukupne Glu pri insulinskoj stimulaciji i Glu se u njih inkorporira i skladišti u vidu glikogena. Glu u ćelije ulazi uz pomoć proteina nosača koji olakšavaju transport Glu kroz ćelijsku membranu i identifikovani su kao glukozni transporteri (GLUT). U ćelijama SM, lokalizovani su GLUT1 i GLUT4. INS stimulisano preuzimanje Glu u mišićnim ćelijama posredovano je translokacijom GLUT4 na površinu ćelijske membrane, dok GLUT1 posreduje u preuzimanju Glu u mišićne ćelije pri bazalnim uslovima. Poremećaji u mehanizmima koji su odgovorni za ovu translokaciju vode insulinskoj rezistenciji. Periferna insulinska resistencija koja uključuje poremećaje transporta Glu u adipocitima i SM, ključni je faktor u patogenezi Diabetesa Mellitusa tipa 2 (DMT2). S obzirom na to da SM preuzimaju najveći deo ukupne Glu, insulinska rezistencija u SM od velikog je značaja za razvoj DMT2 i može se javiti na tri nivoa: na nivou transporta Glu, fosforilacije Glu i na nivou sinteze glikogena. Transport Glu je osnovni korak u preuzimanju Glu u SM pri insulinskoj stimulaciji i ograničavajući je faktor za celokupan metabolizam Glu u organizmu.",
journal = "Timočki medicinski glasnik",
title = "Insulin signaling pathway in skeletal muscles, Signalni put insulina u ćelijama skeletnih mišića",
volume = "31",
number = "4",
pages = "180-185",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10334"
}
Sudar, E., Velebit, J.,& Isenović, E. R.. (2006). Insulin signaling pathway in skeletal muscles. in Timočki medicinski glasnik, 31(4), 180-185.
https://hdl.handle.net/21.15107/rcub_vinar_10334
Sudar E, Velebit J, Isenović ER. Insulin signaling pathway in skeletal muscles. in Timočki medicinski glasnik. 2006;31(4):180-185.
https://hdl.handle.net/21.15107/rcub_vinar_10334 .
Sudar, Emina, Velebit, Jelena, Isenović, Esma R., "Insulin signaling pathway in skeletal muscles" in Timočki medicinski glasnik, 31, no. 4 (2006):180-185,
https://hdl.handle.net/21.15107/rcub_vinar_10334 .