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Article: Vliianie érastina i G3139 na mitokhondrii pecheni krys pri khronicheskoĭ alkogol'noĭ intoksikatsii.

Baburina, Yu L / Zvyagina, A I / Odinokova, I V / Krestinina, O V

2023 Volume 69, Issue 1, Page(s) 62–71

Abstract: The effect of modulators of VDAC channels - G3139 and erastin on the mitochondrial permeability transition pore (mPTP) functioning and changes in the content of proteins involved in regulation of mPTP (VDAC, CNPase, and TSPO) has been investigated in ... ...

Title translation	Effect of erastin and G3139 on rat liver mitochondria in chronic alcoholic intoxication.
Abstract	The effect of modulators of VDAC channels - G3139 and erastin on the mitochondrial permeability transition pore (mPTP) functioning and changes in the content of proteins involved in regulation of mPTP (VDAC, CNPase, and TSPO) has been investigated in liver mitochondria of rats with chronic alcohol intoxication. It was shown that the mitochondria of rats treated with ethanol were more sensitive to mPTP induction. Moreover, ethanol induced changes in the expression of mPTP regulator proteins. G3139 and erastin were also able to influence the studied mitochondrial parameters, and they increased their effect in the liver mitochondria of rats treated with ethanol, as compared to the mitochondria of control rats. We hypothesize that the results of this study may help to elucidate the mechanisms of chronic action of ethanol on mitochondria and contribute to the development of new therapeutic strategies for treating the consequences of ethanol-related diseases.
MeSH term(s)	Animals ; Rats ; Mitochondria, Liver ; Alcoholism ; Mitochondria ; Ethanol
Chemical Substances	erastin ; oblimersen (85J5ZP6YSL) ; Ethanol (3K9958V90M)
Language	Russian
Publishing date	2023-03-01
Publishing country	Russia (Federation)
Document type	English Abstract ; Journal Article
ZDB-ID	2130758-1
ISSN	2310-6905 ; 2310-6972 ; 0042-8809
ISSN (online)	2310-6905
ISSN	2310-6972 ; 0042-8809
DOI	10.18097/PBMC20236901062
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Article ; Online: TR-57 Treatment of SUM159 Cells Induces Mitochondrial Dysfunction without Affecting Membrane Potential.

Mishukov, Artem / Mndlyan, Ekaterina / Berezhnov, Alexey V / Kobyakova, Margarita / Lomovskaya, Yana / Holmuhamedov, Ekhson / Odinokova, Irina

International journal of molecular sciences

2024 Volume 25, Issue 2

Abstract: ... I, II, III and IV proteins, respectively. The content of the F ...

Abstract	Recent works identified ClpXP, mitochondrial caseinolytic protease, as the only target of imipridones, a new class of antitumor agents. Our study of the mechanism of imipridone derivative TR-57 action in SUM159 human breast cancer cells demonstrated mitochondrial fragmentation, degradation of mitochondrial mtDNA and mitochondrial dysfunction due to inhibition of Complex I and Complex II activity. Complete inhibition of oxidative phosphorylation accompanied 90, 94, 88 and 87% decreases in the content of Complex I, II, III and IV proteins, respectively. The content of the F
MeSH term(s)	Humans ; Mitochondria ; Membrane Potential, Mitochondrial ; Adenosine Triphosphatases ; Adenine Nucleotide Translocator 2 ; Electron Transport Complex I ; Mitochondrial Diseases ; Adenosine Triphosphate
Chemical Substances	Adenosine Triphosphatases (EC 3.6.1.-) ; Adenine Nucleotide Translocator 2 ; Electron Transport Complex I (EC 7.1.1.2) ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2024-01-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25021193
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Article ; Online: Pro-Inflammatory Activation Suppresses TRAIL-induced Apoptosis of Acute Myeloid Leukemia Cells.

Kobyakova, Margarita I / Senotov, Anatoly S / Krasnov, Kirill S / Lomovskaya, Yana V / Odinokova, Irina V / Kolotova, Anastasia A / Ermakov, Artem M / Zvyagina, Alena I / Fadeeva, Irina S / Fetisova, Elena I / Akatov, Vladimir S / Fadeev, Roman S

Biochemistry. Biokhimiia

2024 Volume 89, Issue 3, Page(s) 431–440

Abstract: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) is a promising agent for treatment of AML due to its specific apoptosis-inducing effect on tumor cells but not normal cells. However, emergence of resistance to TRAIL in the AML cells ... ...

Abstract	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) is a promising agent for treatment of AML due to its specific apoptosis-inducing effect on tumor cells but not normal cells. However, emergence of resistance to TRAIL in the AML cells limits its potential as an antileukemic agent. Previously, we revealed increase in the resistance of the human AML THP-1 cells to the TRAIL-induced death during their LPS-dependent proinflammatory activation and in the in vitro model of LPS-independent proinflammatory activation - in a long-term high-density cell culture. In this study, we investigated mechanisms of this phenomenon using Western blot analysis, caspase 3 enzymatic activity analysis, quantitative reverse transcription-PCR, and flow cytometry. The results showed that the increased resistance to the TRAIL-induced cell death of AML THP-1 cells during their pro-inflammatory activation is associated with the decrease in the surface expression of the proapoptotic receptors TRAIL-R1/DR4 and TRAIL-R2/DR5, as well as with the increased content of members of the IAPs family - Livin and cIAP2. The results of this article open up new insights into the role of inflammation in formation of the resistance of AML cells to the action of mediators of antitumor immunity, in particular TRAIL.
MeSH term(s)	Humans ; TNF-Related Apoptosis-Inducing Ligand/metabolism ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Leukemia, Myeloid, Acute/drug therapy ; Apoptosis/drug effects ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics ; THP-1 Cells ; Inflammation/metabolism ; Lipopolysaccharides/pharmacology ; Caspase 3/metabolism
Chemical Substances	TNF-Related Apoptosis-Inducing Ligand ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Lipopolysaccharides ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2024-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297924030040
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Article ; Online: Dynamics of the permeability transition pore size in isolated mitochondria and mitoplasts.

Kruglov, Alexey G / Kharechkina, Ekaterina S / Nikiforova, Anna B / Odinokova, Irina V / Kruglova, Svetlana A

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2021 Volume 35, Issue 8, Page(s) e21764

Abstract: The size of the permeability transition pore (PTP) is accepted to be ≤1.5 kDa. However, different authors reported values from 650 to 4000 Da. The present study is focused on the variability of the average PTP size in and between mitochondrial samples, ... ...

Abstract	The size of the permeability transition pore (PTP) is accepted to be ≤1.5 kDa. However, different authors reported values from 650 to 4000 Da. The present study is focused on the variability of the average PTP size in and between mitochondrial samples, its reasons and relations with PTP dynamics. Measurement of PTP size by the standard method revealed its 500 Da-range variability between mitochondrial samples. Sequential measurements in the same sample showed that the PTP size tends to grow with time and Ca
MeSH term(s)	Calcium/chemistry ; Humans ; Mitochondria/chemistry ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/chemistry ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Membranes/chemistry ; Mitochondrial Membranes/metabolism
Chemical Substances	Mitochondrial Membrane Transport Proteins ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-07-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202100596R
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Article ; Online: Investigation of the calcium-induced activation of the bacteriophage T5 peptidoglycan hydrolase promoting host cell lysis.

Kovalenko, Angelina O / Chernyshov, Sergei V / Kutyshenko, Victor P / Molochkov, Nikolai V / Prokhorov, Dmitry A / Odinokova, Irina V / Mikoulinskaia, Galina V

Metallomics : integrated biometal science

2019 Volume 11, Issue 4, Page(s) 799–809

Abstract: Peptidoglycan hydrolase of bacteriophage T5 (EndoT5) is a Ca2+-dependent l-alanyl-d-glutamate peptidase, although the mode of Ca2+ binding and its physiological significance remain obscure. Site-directed mutagenesis was used to elucidate the role of the ... ...

Abstract	Peptidoglycan hydrolase of bacteriophage T5 (EndoT5) is a Ca2+-dependent l-alanyl-d-glutamate peptidase, although the mode of Ca2+ binding and its physiological significance remain obscure. Site-directed mutagenesis was used to elucidate the role of the polar amino acids of the mobile loop of EndoT5 (111-130) in Ca2+ binding. The mutant proteins were purified to electrophoretic homogeneity, the overall structures were characterized by circular dichroism, and the calcium dissociation constants were determined via NMR spectroscopy. The data suggest that polar amino acids D113, N115, and S117 of EndoT5 are involved in the coordination of calcium ions by forming the core of the EF-like Ca2+-binding loop while the charged residues D122 and E123 of EndoT5 contribute to maintaining the loop net charge density. The results suggest that Ca2+ binding to the EndoT5 molecule could be essential for the stabilization of the long mobile loop in the catalytically active "open" conformation. The possible mechanism of Ca2+ regulation of EndoT5 activity during bacteriophage T5's life cycle through the Ca2+ concentration difference between the cytoplasm and the periplasm of the host bacteria cell has been discussed. The study reveals valuable insight into the role of calcium in the regulation of phage-induced bacterial lysis.
MeSH term(s)	Calcium/metabolism ; Enzyme Activation ; Escherichia coli/cytology ; Escherichia coli/virology ; Models, Molecular ; N-Acetylmuramoyl-L-alanine Amidase/metabolism ; T-Phages/enzymology ; T-Phages/metabolism ; Viral Proteins/metabolism
Chemical Substances	Viral Proteins ; N-Acetylmuramoyl-L-alanine Amidase (EC 3.5.1.28) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-03-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2474317-3
ISSN	1756-591X ; 1756-5901
ISSN (online)	1756-591X
ISSN	1756-5901
DOI	10.1039/c9mt00020h
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Article ; Online: Regulation of permeability transition pore opening in mitochondria by external NAD(H).

Kharechkina, Ekaterina S / Nikiforova, Anna B / Teplova, Vera V / Odinokova, Irina V / Krestinina, Olga V / Baburina, Yulia L / Kruglova, Svetlana A / Kruglov, Alexey G

Biochimica et biophysica acta. General subjects

2019 Volume 1863, Issue 5, Page(s) 771–783

Abstract: Background: The opening of the permeability transition pore (PTP) in mitochondria plays a critical role in the pathogenesis of numerous diseases. Mitochondrial matrix pyridine nucleotides are potent regulators of the PTP, but the role of ... ...

Abstract	Background: The opening of the permeability transition pore (PTP) in mitochondria plays a critical role in the pathogenesis of numerous diseases. Mitochondrial matrix pyridine nucleotides are potent regulators of the PTP, but the role of extramitochondrial nucleotides is unclear. Methods: The PTP opening was explored in isolated mitochondria and mitochondria in permeabilized differentiated and undifferentiated cells in the presence of added NAD(P)(H) in combination with Mg Results: Added NAD(H) and AN, but not NADP(H), inhibited the PTP opening with comparable potency. PTP suppression required neither NAD(H) oxidation nor reduction. The protective effects of NAD(H) and cyclosporin A were synergistic, and the effects of NAD(H) and millimolar AN were additive. The conformation-specific ANT inhibitors were unable to cancel the protective effect of NADH even under total ANT inhibition. Besides, NAD(H) activated the efflux of mitochondrial AN via ANT. VDAC ligand (Mg Conclusions: The study revealed a novel mechanism of PTP regulation by external (cytosolic) NAD(H) through the allosteric site in the OM or the intermembrane space. General significance: The mechanism might contribute to the resistance of differentiated cells under different pathological conditions including ischemia/reperfusion.
MeSH term(s)	Animals ; Cell Line, Tumor ; HEK293 Cells ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Mice ; Mitochondria, Heart/metabolism ; Mitochondrial Membrane Transport Proteins/isolation & purification ; Mitochondrial Membrane Transport Proteins/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; NAD/metabolism ; Rats
Chemical Substances	Mitochondrial Membrane Transport Proteins ; mitochondrial permeability transition pore ; NAD (0U46U6E8UK)
Language	English
Publishing date	2019-02-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2019.01.003
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Article ; Online: Interaction of myelin basic protein and 2',3'-cyclic nucleotide phosphodiesterase with mitochondria.

Baburina, Yu L / Gordeeva, A E / Moshkov, D A / Krestinina, O V / Azarashvili, A A / Odinokova, I V / Azarashvili, T S

Biochemistry. Biokhimiia

2014 Volume 79, Issue 6, Page(s) 555–565

Abstract: The content and distribution of myelin basic protein (MBP) isoforms (17 and 21.5 kDa) as well as 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase) were determined in mitochondrial fractions (myelin fraction, synaptic and nonsynaptic mitochondria) ... ...

Abstract	The content and distribution of myelin basic protein (MBP) isoforms (17 and 21.5 kDa) as well as 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase) were determined in mitochondrial fractions (myelin fraction, synaptic and nonsynaptic mitochondria) obtained after separation of brain mitochondria by Percoll density gradient. All the fractions could accumulate calcium, maintain membrane potential, and initiate the opening of the permeability transition pore (mPTP) in response to calcium overloading. Native mitochondria and structural contacts between membranes of myelin and mitochondria were found in the myelin fraction associated with brain mitochondria. Using Western blot, it was shown that addition of myelin fraction associated with brain mitochondria to the suspension of liver mitochondria can lead to binding of CNPase and MBP, present in the fraction with liver mitochondria under the conditions of both closed and opened mPTP. However, induction of mPTP opening in liver mitochondria was prevented in the presence of myelin fraction associated with brain mitochondria (Ca2+ release rate was decreased 1.5-fold, calcium retention time was doubled, and swelling amplitude was 2.8-fold reduced). These results indicate possible protective properties of MBP and CNPase.
MeSH term(s)	2',3'-Cyclic-Nucleotide Phosphodiesterases/chemistry ; 2',3'-Cyclic-Nucleotide Phosphodiesterases/metabolism ; Animals ; Brain/metabolism ; Calcium/metabolism ; Male ; Mitochondria/metabolism ; Mitochondria, Liver/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Myelin Basic Protein/chemistry ; Myelin Basic Protein/metabolism ; Protein Isoforms/chemistry ; Protein Isoforms/metabolism ; Protein Structure, Tertiary ; Rats ; Rats, Wistar
Chemical Substances	Mitochondrial Membrane Transport Proteins ; Myelin Basic Protein ; Protein Isoforms ; mitochondrial permeability transition pore ; 2',3'-Cyclic-Nucleotide Phosphodiesterases (EC 3.1.4.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297914060091
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Article ; Online: Mitochondrial mechanisms of death responses in pancreatitis.

Odinokova, Irina V / Sung, Kai-Feng / Mareninova, Olga A / Hermann, Kip / Gukovsky, Ilya / Gukovskaya, Anna S

Journal of gastroenterology and hepatology

2008 Volume 23 Suppl 1, Page(s) S25–30

Abstract: Pancreatitis is a severe and frequently lethal disorder, a major cause of which is alcohol abuse. Parenchymal cell death is a major complication of pancreatitis. In experimental models of acute pancreatitis, acinar cells have been shown to die through ... ...

Abstract	Pancreatitis is a severe and frequently lethal disorder, a major cause of which is alcohol abuse. Parenchymal cell death is a major complication of pancreatitis. In experimental models of acute pancreatitis, acinar cells have been shown to die through both necrosis and apoptosis, the two principal pathways of cell death. The severity of experimental acute pancreatitis correlates directly with the extent of necrosis and inversely with apoptosis. Thus, understanding the regulation of apoptosis and necrosis is becoming exceedingly important in investigations of the pathogenesis and treatment of pancreatitis. Over the past decade, the mitochondria have emerged as a master regulator of cell death in various physiological and pathological processes. Release of mitochondrial cytochrome c into the cytosol is a central event in apoptosis, whereas mitochondrial depolarization resulting in ATP depletion leads to necrosis. The present review focuses on the mitochondrial mechanisms of death responses in pancreatitis, with emphasis on mitochondrial membrane permeabilization and its role in the balance between apoptosis and necrosis in acute pancreatitis, and alcohol's effects on death responses of pancreatitis.
MeSH term(s)	Apoptosis ; Cell Death ; Humans ; Mitochondria/physiology ; Necrosis ; Pancreatitis/metabolism ; Pancreatitis/pathology
Language	English
Publishing date	2008-03
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	632882-9
ISSN	1440-1746 ; 0815-9319
ISSN (online)	1440-1746
ISSN	0815-9319
DOI	10.1111/j.1440-1746.2007.05271.x
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Article: Phosphorylation of a low-molecular-weight polypeptide in rat liver mitochondria and dependence of its phosphorylation on mitochondrial functional state.

Azarashvili, T S / Odinokova, I V / Evtodienko, Y V

Biochemistry. Biokhimiia

1999 Volume 64, Issue 5, Page(s) 556–560

Abstract: We show that incubation of rat liver mitochondria in the presence of [gamma-32P]ATP results in cAMP-dependent phosphorylation of a low-molecular-weight (3.5-kD) polypeptide (LMWP). This component is tightly bound to the mitochondrial membrane. It is not ... ...

Abstract	We show that incubation of rat liver mitochondria in the presence of [gamma-32P]ATP results in cAMP-dependent phosphorylation of a low-molecular-weight (3.5-kD) polypeptide (LMWP). This component is tightly bound to the mitochondrial membrane. It is not released into solution after freezing and subsequent thawing of the mitochondrial suspension and does not incorporate 32P from [gamma-32P]ATP in the presence of uncouplers of oxidative phosphorylation. Inhibition of adenine nucleotide transport into the mitochondrial matrix by carboxyatractyloside suppresses phosphorylation of the LMWP. Moderate Ca2+ loading of mitochondria increases both phosphorylation and dephosphorylation of the LMWP. Chelation of Ca2+ by incubation in the presence of EGTA suppresses incorporation of 32P into the LMWP.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/physiology ; Molecular Weight ; Oxidative Phosphorylation ; Peptides/chemistry ; Peptides/metabolism ; Phosphorus Radioisotopes ; Rats ; Rats, Wistar
Chemical Substances	Peptides ; Phosphorus Radioisotopes ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	1999-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
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Article ; Online: Inflammatory cells regulate p53 and caspases in acute pancreatitis.

Nakamura, Yuji / Do, Jae Hyuk / Yuan, Jingzhen / Odinokova, Irina V / Mareninova, Olga / Gukovskaya, Anna S / Pandol, Stephen J

American journal of physiology. Gastrointestinal and liver physiology

2009 Volume 298, Issue 1, Page(s) G92–100

Abstract: The inflammatory response during pancreatitis regulates necrotic and apoptotic rates of parenchymal cells. Neutrophil depletion by use of anti-polymorphonuclear serum (anti-PMN) increases apoptosis in experimental pancreatitis but the mechanism has not ... ...

Abstract	The inflammatory response during pancreatitis regulates necrotic and apoptotic rates of parenchymal cells. Neutrophil depletion by use of anti-polymorphonuclear serum (anti-PMN) increases apoptosis in experimental pancreatitis but the mechanism has not been determined. Our study was designed to investigate signaling mechanisms in pancreatic parenchymal cells regulating death responses with neutrophil depletion. Rats were neutrophil depleted with anti-PMN treatment. Then cerulein pancreatitis was induced, followed by measurements of apoptosis signaling pathways. There was greater activation of executioner caspases-3 in the pancreas with anti-PMN treatment compared with control. There were no differences between these groups of animals in mitochondrial cytochrome c release or in activities of initiator caspase-8 and -9. However, there was greater activation of caspase-2 with anti-PMN treatment during cerulein pancreatitis. The upstream regulation of caspases-2 includes p53, which was increased; the p53 negative regulator, Mdm2, was decreased by anti-PMN treatment during cerulein pancreatitis. In vitro experiments using isolated pancreatic acinar cells a pharmacological inhibitor of Mdm2 increased caspase-2/-3 activities, and an inhibitor of p53 decreased these activities during cholecystokinin-8 treatment. Furthermore, experiments using the AR42J cell line Mdm2 small interfering RNA (siRNA) increased caspase-2/-3 activities, and p53 siRNA decreased these activities during cholecystokinin-8 treatment. These results suggest that during acute pancreatitis the inflammatory response inhibits apoptosis. The mechanism of this inhibition involves caspase-2 and its upstream regulation by p53 and Mdm2. Because previous findings indicate that promotion of apoptosis decreases necrosis and severity of pancreatitis, these results suggest that strategies to inhibit Mdm2 or activate p53 will have beneficial effects for treatment of pancreatitis.
MeSH term(s)	Acute Disease ; Animals ; Apoptosis/physiology ; Caspase 3/metabolism ; Caspase 8/metabolism ; Caspase 9/metabolism ; Caspases/metabolism ; Cells, Cultured ; Ceruletide/pharmacology ; Cysteine Endopeptidases/metabolism ; Cytochromes c/metabolism ; Disease Models, Animal ; Male ; Necrosis ; Neutrophils/immunology ; Neutrophils/metabolism ; Pancreatitis/chemically induced ; Pancreatitis/immunology ; Pancreatitis/metabolism ; Pancreatitis/pathology ; Proto-Oncogene Proteins c-mdm2/genetics ; Proto-Oncogene Proteins c-mdm2/metabolism ; RNA, Small Interfering ; Rats ; Rats, Sprague-Dawley ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	RNA, Small Interfering ; Tumor Suppressor Protein p53 ; Ceruletide (888Y08971B) ; Cytochromes c (9007-43-6) ; Mdm2 protein, rat (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Casp2 protein, rat (EC 3.4.22.-) ; Casp3 protein, rat (EC 3.4.22.-) ; Casp8 protein, rat (EC 3.4.22.-) ; Casp9 protein, rat (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-) ; Caspases (EC 3.4.22.-) ; Cysteine Endopeptidases (EC 3.4.22.-)
Language	English
Publishing date	2009-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00324.2009
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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