TY  - JOUR
AU  - Đorđević, Marija
AU  - Paunović, Verica
AU  - Jovanović Tucović, Maja
AU  - Tolić, Anja
AU  - Rajić, Jovana
AU  - Dinić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Grdović, Nevena
AU  - Mihailović, Mirjana
AU  - Marković, Ivanka
AU  - Arambašić Jovanović, Jelena
AU  - Vidaković, Melita
PY  - 2022
UR  - https://www.mdpi.com/2076-3417/12/15/7938
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5102
AB  - An efficient transfection is a crucial step for the introduction of epigenetic modification in host cells, and there is a need for an optimized transfection process for individual model systems separately. Mouse pancreatic αTC1-6 cells, which act as an attractive model system for epigenetic cell reprogramming and diabetes treatment, were transiently transfected with two different transfection methods: the chemical method with polyethyleneimine (PEI) and nucleofection as a physical transfection method. Flow cytometry and fluorescent microscopy examination of GFP expression showed that transfection efficiency was affected by the size of plasmids using both transfection methods. Subsequently, the Cas9 mRNA expression confirmed successful transfection with EpiCRISPR plasmid, whereas the cell physiology remained unchanged. The adjusted nucleofection protocol for αTC1-6 cells transfected with an EpiCRISPR mix of plasmids reached 71.1% of GFP-positive transfected cells on the fifth post-transfection day and proved to be much more efficient than the 3.8% GFP-positive PEI transfected cells. Modifying the protocol, we finally specify CM-156 program and SF 4D-Nucleofector X Solutions for Amaxa™ nucleofection as a method of choice for alpha TC1-6 cell line transfection.
PB  - Basel: MDPI
T2  - Applied Sciences
T1  - Nucleofection as an Efficient Method for Alpha TC1-6 Cell Line Transfection
IS  - 15
VL  - 12
DO  - 10.3390/app12157938
SP  - 7938
ER  - 

@article{
author = "Đorđević, Marija and Paunović, Verica and Jovanović Tucović, Maja and Tolić, Anja and Rajić, Jovana and Dinić, Svetlana and Uskoković, Aleksandra and Grdović, Nevena and Mihailović, Mirjana and Marković, Ivanka and Arambašić Jovanović, Jelena and Vidaković, Melita",
year = "2022",
abstract = "An efficient transfection is a crucial step for the introduction of epigenetic modification in host cells, and there is a need for an optimized transfection process for individual model systems separately. Mouse pancreatic αTC1-6 cells, which act as an attractive model system for epigenetic cell reprogramming and diabetes treatment, were transiently transfected with two different transfection methods: the chemical method with polyethyleneimine (PEI) and nucleofection as a physical transfection method. Flow cytometry and fluorescent microscopy examination of GFP expression showed that transfection efficiency was affected by the size of plasmids using both transfection methods. Subsequently, the Cas9 mRNA expression confirmed successful transfection with EpiCRISPR plasmid, whereas the cell physiology remained unchanged. The adjusted nucleofection protocol for αTC1-6 cells transfected with an EpiCRISPR mix of plasmids reached 71.1% of GFP-positive transfected cells on the fifth post-transfection day and proved to be much more efficient than the 3.8% GFP-positive PEI transfected cells. Modifying the protocol, we finally specify CM-156 program and SF 4D-Nucleofector X Solutions for Amaxa™ nucleofection as a method of choice for alpha TC1-6 cell line transfection.",
publisher = "Basel: MDPI",
journal = "Applied Sciences",
title = "Nucleofection as an Efficient Method for Alpha TC1-6 Cell Line Transfection",
number = "15",
volume = "12",
doi = "10.3390/app12157938",
pages = "7938"
}

Đorđević, M., Paunović, V., Jovanović Tucović, M., Tolić, A., Rajić, J., Dinić, S., Uskoković, A., Grdović, N., Mihailović, M., Marković, I., Arambašić Jovanović, J.,& Vidaković, M.. (2022). Nucleofection as an Efficient Method for Alpha TC1-6 Cell Line Transfection. in Applied Sciences
Basel: MDPI., 12(15), 7938.
https://doi.org/10.3390/app12157938

Đorđević M, Paunović V, Jovanović Tucović M, Tolić A, Rajić J, Dinić S, Uskoković A, Grdović N, Mihailović M, Marković I, Arambašić Jovanović J, Vidaković M. Nucleofection as an Efficient Method for Alpha TC1-6 Cell Line Transfection. in Applied Sciences. 2022;12(15):7938.
doi:10.3390/app12157938 .

Đorđević, Marija, Paunović, Verica, Jovanović Tucović, Maja, Tolić, Anja, Rajić, Jovana, Dinić, Svetlana, Uskoković, Aleksandra, Grdović, Nevena, Mihailović, Mirjana, Marković, Ivanka, Arambašić Jovanović, Jelena, Vidaković, Melita, "Nucleofection as an Efficient Method for Alpha TC1-6 Cell Line Transfection" in Applied Sciences, 12, no. 15 (2022):7938,
https://doi.org/10.3390/app12157938 . .

TY  - CONF
AU  - Jeremić, Marija
AU  - Jovanović, Maja
AU  - Tovilović-Kovačević, Gordana
AU  - Harhaji-Trajković, Ljubica
AU  - Zogović, Nevena
AU  - Vukojević, Milica
AU  - Kostić, Vladimir
AU  - Marković, Ivanka D.
AU  - Trajković, Vladimir
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4450
AB  - Alpha-synuclein (ASYN) is regarded as one of the key culprits in
pathogenesis of synucleinopathies, including Parkinson’s disease,
and impaired regulation of autophagy is associated with the
ASYN aggregation. Autophagy is regulated by complex mechanisms,
including AMP activated protein kinase (AMPK), a key
energy sensor regulating cellular metabolism to maintain energy
homeostasis. The aim of our study was to investigate the role of
AMPK and autophagy in neurotoxic effect of secreted ASYN, as
well as dopamine-modified and nitrated recombinant wild-type
ASYN oligomers, on retinoic acid (RA)-differentiated SH-SY5Y
cells. The culture supernatant from neuroblastoma cells stably
expressing wt ASYN was collected and used as conditioned medium (CM). The presence of wt ASYN in CM was confirmed
by immunoblot, following lyophilisation. The CM, as well as
recombinant dopamine-modified or nitrated ASYN, all reduced
viability in differentiated SH-SY5Y cells. This decrease in viability
was accompanied by reduced AMPK activation, increased
conversion of LC3-I to LC3-II and increase in Beclin-1 level, as
demonstrated by immunoblot. Pharmacological activators of
AMPK and autophagy (metformin and AICAR) significantly
increased the cells’ viability in the presence of CM and modified
ASYN forms. Level of AMPK-activated pULK was reduced in
presence of CM, but pharmacological activators of AMPK
reversed that effect. Pharmacological inhibitors of autophagy,
further reduced cell viability in the presence of extracellular
ASYN. The shRNA-mediated LC3 downregulation, as well as
the RNA interference-mediated knockdown of ATG7 gene, both
important for autophagosome biogenesis/maturation, increased
sensitivity of SH-SY5Y cells to the extracellular ASYN-induced
toxicity. These data demonstrate the protective role of AMPK
and autophagy against the toxicity of extracellular ASYN, suggesting
that their modulation may be a promising neuroprotective
strategy in Parkinson’s disease.
PB  - Hoboken: Wiley
C3  - FEBS OpenBio
T1  - Neurotoxic effect of extracellular alpha-synuclein can be alleviated by AMPK and autophagy
IS  - Supplement 1
VL  - 11
SP  - 463
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_4450
ER  - 

@conference{
author = "Jeremić, Marija and Jovanović, Maja and Tovilović-Kovačević, Gordana and Harhaji-Trajković, Ljubica and Zogović, Nevena and Vukojević, Milica and Kostić, Vladimir and Marković, Ivanka D. and Trajković, Vladimir",
year = "2021",
abstract = "Alpha-synuclein (ASYN) is regarded as one of the key culprits in
pathogenesis of synucleinopathies, including Parkinson’s disease,
and impaired regulation of autophagy is associated with the
ASYN aggregation. Autophagy is regulated by complex mechanisms,
including AMP activated protein kinase (AMPK), a key
energy sensor regulating cellular metabolism to maintain energy
homeostasis. The aim of our study was to investigate the role of
AMPK and autophagy in neurotoxic effect of secreted ASYN, as
well as dopamine-modified and nitrated recombinant wild-type
ASYN oligomers, on retinoic acid (RA)-differentiated SH-SY5Y
cells. The culture supernatant from neuroblastoma cells stably
expressing wt ASYN was collected and used as conditioned medium (CM). The presence of wt ASYN in CM was confirmed
by immunoblot, following lyophilisation. The CM, as well as
recombinant dopamine-modified or nitrated ASYN, all reduced
viability in differentiated SH-SY5Y cells. This decrease in viability
was accompanied by reduced AMPK activation, increased
conversion of LC3-I to LC3-II and increase in Beclin-1 level, as
demonstrated by immunoblot. Pharmacological activators of
AMPK and autophagy (metformin and AICAR) significantly
increased the cells’ viability in the presence of CM and modified
ASYN forms. Level of AMPK-activated pULK was reduced in
presence of CM, but pharmacological activators of AMPK
reversed that effect. Pharmacological inhibitors of autophagy,
further reduced cell viability in the presence of extracellular
ASYN. The shRNA-mediated LC3 downregulation, as well as
the RNA interference-mediated knockdown of ATG7 gene, both
important for autophagosome biogenesis/maturation, increased
sensitivity of SH-SY5Y cells to the extracellular ASYN-induced
toxicity. These data demonstrate the protective role of AMPK
and autophagy against the toxicity of extracellular ASYN, suggesting
that their modulation may be a promising neuroprotective
strategy in Parkinson’s disease.",
publisher = "Hoboken: Wiley",
journal = "FEBS OpenBio",
title = "Neurotoxic effect of extracellular alpha-synuclein can be alleviated by AMPK and autophagy",
number = "Supplement 1",
volume = "11",
pages = "463",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_4450"
}

Jeremić, M., Jovanović, M., Tovilović-Kovačević, G., Harhaji-Trajković, L., Zogović, N., Vukojević, M., Kostić, V., Marković, I. D.,& Trajković, V.. (2021). Neurotoxic effect of extracellular alpha-synuclein can be alleviated by AMPK and autophagy. in FEBS OpenBio
Hoboken: Wiley., 11(Supplement 1), 463.
https://hdl.handle.net/21.15107/rcub_ibiss_4450

Jeremić M, Jovanović M, Tovilović-Kovačević G, Harhaji-Trajković L, Zogović N, Vukojević M, Kostić V, Marković ID, Trajković V. Neurotoxic effect of extracellular alpha-synuclein can be alleviated by AMPK and autophagy. in FEBS OpenBio. 2021;11(Supplement 1):463.
https://hdl.handle.net/21.15107/rcub_ibiss_4450 .

Jeremić, Marija, Jovanović, Maja, Tovilović-Kovačević, Gordana, Harhaji-Trajković, Ljubica, Zogović, Nevena, Vukojević, Milica, Kostić, Vladimir, Marković, Ivanka D., Trajković, Vladimir, "Neurotoxic effect of extracellular alpha-synuclein can be alleviated by AMPK and autophagy" in FEBS OpenBio, 11, no. Supplement 1 (2021):463,
https://hdl.handle.net/21.15107/rcub_ibiss_4450 .

TY  - CONF
AU  - Vučićević, Ljubica
AU  - Misirkić Marjanović, Maja
AU  - Ćirić, Darko
AU  - Martinović, Tamara
AU  - Jovanović, Maja
AU  - Isaković, Aleksandra
AU  - Marković, Ivanka
AU  - Zogović, Nevena
AU  - Foretz, Mark
AU  - Rabanal-Ruiz, Yoana
AU  - Korolchuk, Viktor
AU  - Trajković, Vladimir
PY  - 2019
UR  - https://www.fens.org/news-activities/fens-and-societies-calendar/meeting-event/fens-regional-meeting-2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6357
AB  - We investigated the effect of excitotoxic glutamate on nutrient starvation-induced autophagy, a process of lysosome-mediated degradation of cellular macromolecules and organelles. Incubation of SH-SY5Y human neuroblastoma cell line in glucose/amino acid/serum-free Hank Balanced Salt solution synergized with glutamate in causing energy stress and excitotoxic necrosis. Glutamate inhibited starvation-induced autophagy, as demonstrated by decreased intracellular acidification, lower LC3 punctuation, reduced conversion of LC3-I to LC3-II, reduced expression of autophagy activators beclin-1 and ATG5, increased
levels of the selective autophagic target NBR1, and decline in the number of autophagic vesicles observed by transmission electron microscopy. NMDA antagonist memantine restored LC3B-II accumulation in starved cells exposed to glutamate, indicating that glutamate exerts its inhibitory role on autophagy by activating NMDA receptors. The modulation of mTOR, the negative regulator of autophagy, was not responsible for glutamate-mediated autophagy inhibition during starvation. On the other hand, glutamate downregulated starvation-induced activation of the intracellular energy sensor AMP-activated protein
kinase (AMPK). This was associated with reduced mRNA expression of autophagy transcription factors FOXO3 and ATF4, as well as molecules involved in autophagy process (ULK1, ATG13, FIP200, ATG14, beclin-1, ATG5, ATG12, SQSTM1). The ability of glutamate to repress transcription of autophagy genes in starved cells was partly mediated by AMPK downregulation. Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, as well as genetic or pharmacological autophagy induction by TFEB overexpression or lithium chloride, rescued cells from glutamate-mediated excitoxicity. These data indicate that transcriptional inhibition of AMPK-dependent autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.
PB  - Belgrade : Serbian Neuroscience Society
C3  - Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
T1  - Autophagy regulation and its role in glutamate excitotoxicity during nutrient stress
SP  - 144
EP  - 144
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6357
ER  - 

@conference{
author = "Vučićević, Ljubica and Misirkić Marjanović, Maja and Ćirić, Darko and Martinović, Tamara and Jovanović, Maja and Isaković, Aleksandra and Marković, Ivanka and Zogović, Nevena and Foretz, Mark and Rabanal-Ruiz, Yoana and Korolchuk, Viktor and Trajković, Vladimir",
year = "2019",
abstract = "We investigated the effect of excitotoxic glutamate on nutrient starvation-induced autophagy, a process of lysosome-mediated degradation of cellular macromolecules and organelles. Incubation of SH-SY5Y human neuroblastoma cell line in glucose/amino acid/serum-free Hank Balanced Salt solution synergized with glutamate in causing energy stress and excitotoxic necrosis. Glutamate inhibited starvation-induced autophagy, as demonstrated by decreased intracellular acidification, lower LC3 punctuation, reduced conversion of LC3-I to LC3-II, reduced expression of autophagy activators beclin-1 and ATG5, increased
levels of the selective autophagic target NBR1, and decline in the number of autophagic vesicles observed by transmission electron microscopy. NMDA antagonist memantine restored LC3B-II accumulation in starved cells exposed to glutamate, indicating that glutamate exerts its inhibitory role on autophagy by activating NMDA receptors. The modulation of mTOR, the negative regulator of autophagy, was not responsible for glutamate-mediated autophagy inhibition during starvation. On the other hand, glutamate downregulated starvation-induced activation of the intracellular energy sensor AMP-activated protein
kinase (AMPK). This was associated with reduced mRNA expression of autophagy transcription factors FOXO3 and ATF4, as well as molecules involved in autophagy process (ULK1, ATG13, FIP200, ATG14, beclin-1, ATG5, ATG12, SQSTM1). The ability of glutamate to repress transcription of autophagy genes in starved cells was partly mediated by AMPK downregulation. Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, as well as genetic or pharmacological autophagy induction by TFEB overexpression or lithium chloride, rescued cells from glutamate-mediated excitoxicity. These data indicate that transcriptional inhibition of AMPK-dependent autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.",
publisher = "Belgrade : Serbian Neuroscience Society",
journal = "Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia",
title = "Autophagy regulation and its role in glutamate excitotoxicity during nutrient stress",
pages = "144-144",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6357"
}

Vučićević, L., Misirkić Marjanović, M., Ćirić, D., Martinović, T., Jovanović, M., Isaković, A., Marković, I., Zogović, N., Foretz, M., Rabanal-Ruiz, Y., Korolchuk, V.,& Trajković, V.. (2019). Autophagy regulation and its role in glutamate excitotoxicity during nutrient stress. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
Belgrade : Serbian Neuroscience Society., 144-144.
https://hdl.handle.net/21.15107/rcub_ibiss_6357

Vučićević L, Misirkić Marjanović M, Ćirić D, Martinović T, Jovanović M, Isaković A, Marković I, Zogović N, Foretz M, Rabanal-Ruiz Y, Korolchuk V, Trajković V. Autophagy regulation and its role in glutamate excitotoxicity during nutrient stress. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia. 2019;:144-144.
https://hdl.handle.net/21.15107/rcub_ibiss_6357 .

Vučićević, Ljubica, Misirkić Marjanović, Maja, Ćirić, Darko, Martinović, Tamara, Jovanović, Maja, Isaković, Aleksandra, Marković, Ivanka, Zogović, Nevena, Foretz, Mark, Rabanal-Ruiz, Yoana, Korolchuk, Viktor, Trajković, Vladimir, "Autophagy regulation and its role in glutamate excitotoxicity during nutrient stress" in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia (2019):144-144,
https://hdl.handle.net/21.15107/rcub_ibiss_6357 .

TY  - CONF
AU  - Jeremić, Marija
AU  - Jovanović, Maja
AU  - Dulović, Marija
AU  - Tovilović-Kovačević, Gordana
AU  - Zogović, Nevena
AU  - Harhaji-Trajković, Ljubica
AU  - Vukojević, Milica
AU  - Kostić, Vladimir
AU  - Marković, Ivanka
AU  - Trajković, Vladimir
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6342
AB  - Alpha-synuclein (ASYN) is regarded as one of the key culprits in pathogenesis of synucleinopathies, including Parkinson’s disease, and impaired regulation of autophagy is associated with the ASYN aggregation. Autophagy is regulated by complex mechanisms, including AMP activated protein kinase (AMPK), a key energy sensor regulating cellular metabolism to maintain energy homeostasis. The aim of our study was to investigate the role of AMPK and autophagy in neurotoxic effect of secreted ASYN, as well as dopamine-modified and nitrated recombinant wild-type ASYN oligomers, on retinoic acid (RA)-differentiated SH-SY5Y cells. The culture supernatant from neuroblastoma cells stably expressing wt ASYN was collected and used as conditioned medium (CM). The presence of wt ASYN in CM was confirmed by immunoblot, following lyophilisation. The CM, as well as recombinant dopamine-modified or nitrated ASYN, all reduced viability in differentiated SH-SY5Y cells. This decrease in viability was accompanied by reduced AMPK activation, increased conversion of LC3-I to LC3-II and increase
in Beclin-1 level, as demonstrated by immunoblot. Pharmacological activators of AMPK and autophagy (metformin and AICAR) significantly increased the cells’ viability in the presence of CM and modified ASYN forms. Pharmacological inhibitors of autophagy (chloroqine, bafilomycin A1 and ammonium-chloride), further reduced cell viability in the presence of extracellular ASYN. The shRNA-mediated LC3 downregulation, as well as the RNA interference-mediated knockdown of ATG7 gene, both important for autophagosome biogenesis/maturation, increased sensitivity of SH-SY5Y cells to the extracellular ASYN-induced toxicity. These data demonstrate the protective role of AMPK and autophagy against the toxicity of extracellular ASYN, suggesting that their modulation may be a promising neuroprotective strategy in Parkinson’s disease.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
T1  - The protective role of AMPK and autophagy in neurotoxicity caused by extracellular alpha-synuclein
SP  - 493
EP  - 493
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6342
ER  - 

@conference{
author = "Jeremić, Marija and Jovanović, Maja and Dulović, Marija and Tovilović-Kovačević, Gordana and Zogović, Nevena and Harhaji-Trajković, Ljubica and Vukojević, Milica and Kostić, Vladimir and Marković, Ivanka and Trajković, Vladimir",
year = "2019",
abstract = "Alpha-synuclein (ASYN) is regarded as one of the key culprits in pathogenesis of synucleinopathies, including Parkinson’s disease, and impaired regulation of autophagy is associated with the ASYN aggregation. Autophagy is regulated by complex mechanisms, including AMP activated protein kinase (AMPK), a key energy sensor regulating cellular metabolism to maintain energy homeostasis. The aim of our study was to investigate the role of AMPK and autophagy in neurotoxic effect of secreted ASYN, as well as dopamine-modified and nitrated recombinant wild-type ASYN oligomers, on retinoic acid (RA)-differentiated SH-SY5Y cells. The culture supernatant from neuroblastoma cells stably expressing wt ASYN was collected and used as conditioned medium (CM). The presence of wt ASYN in CM was confirmed by immunoblot, following lyophilisation. The CM, as well as recombinant dopamine-modified or nitrated ASYN, all reduced viability in differentiated SH-SY5Y cells. This decrease in viability was accompanied by reduced AMPK activation, increased conversion of LC3-I to LC3-II and increase
in Beclin-1 level, as demonstrated by immunoblot. Pharmacological activators of AMPK and autophagy (metformin and AICAR) significantly increased the cells’ viability in the presence of CM and modified ASYN forms. Pharmacological inhibitors of autophagy (chloroqine, bafilomycin A1 and ammonium-chloride), further reduced cell viability in the presence of extracellular ASYN. The shRNA-mediated LC3 downregulation, as well as the RNA interference-mediated knockdown of ATG7 gene, both important for autophagosome biogenesis/maturation, increased sensitivity of SH-SY5Y cells to the extracellular ASYN-induced toxicity. These data demonstrate the protective role of AMPK and autophagy against the toxicity of extracellular ASYN, suggesting that their modulation may be a promising neuroprotective strategy in Parkinson’s disease.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia",
title = "The protective role of AMPK and autophagy in neurotoxicity caused by extracellular alpha-synuclein",
pages = "493-493",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6342"
}

Jeremić, M., Jovanović, M., Dulović, M., Tovilović-Kovačević, G., Zogović, N., Harhaji-Trajković, L., Vukojević, M., Kostić, V., Marković, I.,& Trajković, V.. (2019). The protective role of AMPK and autophagy in neurotoxicity caused by extracellular alpha-synuclein. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 493-493.
https://hdl.handle.net/21.15107/rcub_ibiss_6342

Jeremić M, Jovanović M, Dulović M, Tovilović-Kovačević G, Zogović N, Harhaji-Trajković L, Vukojević M, Kostić V, Marković I, Trajković V. The protective role of AMPK and autophagy in neurotoxicity caused by extracellular alpha-synuclein. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia. 2019;:493-493.
https://hdl.handle.net/21.15107/rcub_ibiss_6342 .

Jeremić, Marija, Jovanović, Maja, Dulović, Marija, Tovilović-Kovačević, Gordana, Zogović, Nevena, Harhaji-Trajković, Ljubica, Vukojević, Milica, Kostić, Vladimir, Marković, Ivanka, Trajković, Vladimir, "The protective role of AMPK and autophagy in neurotoxicity caused by extracellular alpha-synuclein" in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia (2019):493-493,
https://hdl.handle.net/21.15107/rcub_ibiss_6342 .