Role of recombinant mitogen-activated protein kinases JNK and p38 in the regulation of apoptosis in blood mononuclear cells under conditions of oxidative stress in vitro

Ryazantseva, N. V.; Novitsky, V. V.; Chasovskih, N. Yu.; Kaygorodova, E. V.; Starikova, E. G.; Starikov, Yu. V.; Radzivil, T. T.

doi:10.1007/s10517-008-0145-z

Cited by 7 publications

(5 citation statements)

References 8 publications

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“…MAPKs are characterized for having three sequential phosphorylation steps [ 59 ], carried out by three groups of enzymes: MAPK kinase kinase (MAPKKK), for example apoptosis signal-regulating kinase 1 (ASK1) and transforming growth factor-b-activated kinase 1 (TAK1); the MAPK kinase (MAPKK), for example Mitogen-activated ERK (Extracellular Signal-Regulated Kinases) kinase MEK 1 through 7); and MAPK, such as ERK 1/2, JNK, and p38. Mitogen-activated protein kinases are serine/threonine type kinases [ 60 , 61 , 62 , 63 , 64 , 65 ] and possess tyrosine (Tyr) and threonine (Thr) conserved double phosphorylation domains [ 59 ]. They are further divided in three subfamilies according to the amino acid present in both phosphorylation sites.…”

Section: Signal Transduction Pathways In Apoptosismentioning

confidence: 99%

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Apoptosis: Activation and Inhibition in Health and Disease

et al. 2018

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There are many types of cell death, each involving multiple and complex molecular events. Cell death can occur accidentally when exposed to extreme physical, chemical, or mechanical conditions, or it can also be regulated, which involves a genetically coded complex machinery to carry out the process. Apoptosis is an example of the latter. Apoptotic cell death can be triggered through different intracellular signalling pathways that lead to morphological changes and eventually cell death. This is a normal and biological process carried out during maturation, remodelling, growth, and development in tissues. To maintain tissue homeostasis, regulatory, and inhibitory mechanisms must control apoptosis. Paradoxically, these same pathways are utilized during infection by distinct intracellular microorganisms to evade recognition by the immune system and therefore survive, reproduce and develop. In cancer, neoplastic cells inhibit apoptosis, thus allowing their survival and increasing their capability to invade different tissues and organs. The purpose of this work is to review the generalities of the molecular mechanisms and signalling pathways involved in apoptosis induction and inhibition. Additionally, we compile the current evidence of apoptosis modulation during cancer and Leishmania infection as a model of apoptosis regulation by an intracellular microorganism.

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Section: Signal Transduction Pathways In Apoptosismentioning

confidence: 99%

“…This subfamily is composed by the JNK1, JNK2, and JNK3 isoforms; and the ERK subfamily features glutamic acid in between two phosphorylation sites (Thr–Glu-Tyr) and is activated mainly by growth factors. This subfamily is composed of the ERK1 and ERK2 isoforms [ 59 , 60 , 61 , 66 ].…”

Section: Signal Transduction Pathways In Apoptosismentioning

confidence: 99%

Apoptosis: Activation and Inhibition in Health and Disease

et al. 2018

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“…The most prominent example is represented by ML3403, which inhibits the target kinase in the double‐digit nanomolar range and the release of TNF‐α from human whole blood (HWB) in the low‐micromolar range. ML3403 served both as lead compound for further optimization studies and as reference compound in in vitro and in vivo studies . The pharmacokinetic profile of ML3403 was extensively investigated by Kammerer et al .…”

Section: Synthesis Of 245‐tri‐substituted Imidazolesmentioning

confidence: 99%

2‐Alkylsulfanyl‐4(5)‐aryl‐5(4)‐heteroarylimidazoles: An Overview on Synthetic Strategies and Biological Activity

Koch

Ansideri

2017

Archiv der Pharmazie

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2-Alkylsulfanyl-4(5)-aryl-5(4)-heteroarylimidazoles represent an important class of ATP-competitive protein kinase inhibitors, offering the possibility of multiple interactions with different regions of the target enzyme. The necessity of exploring the effects of diverse chemical decorations around the imidazole core prompted the design of several synthetic routes aimed at achieving both efficiency and flexibility. Additionally, the optimization of established protocols and the extensive use of transition metal-catalyzed cross-coupling reactions have been broadening the spectrum of preparative methodologies within the last decade. This review summarizes the progress in the development of synthetic strategies leading to 2-alkylsulfanyl-4(5)-aryl-5(4)-heteroarylimidazoles and 1-alkyl-2-alkylsulfanyl-4(5)-aryl-5(4)-heteroarylimidazoles and offers a glance at the biological activities of this class of compounds.

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“…Stress-activated protein kinase/JNK and ERK are two major pathways of MAPK. Generally, the JNK promotes inflammation, apoptosis, growth, differentiation and oncogenic transformation, whereas ERK is involved in growth, differentiation and development (19)(20)(21). Therefore, we analyzed the effect of NRP-1 siRNA on the MAPK signaling pathway.…”

Section: Rnai-mediated Inhibition Of Nrp-1 Decreases Phosphorylation mentioning

confidence: 99%

RNA interference targeting NRP-1 inhibits human glioma cell proliferation and enhances cell apoptosis

Tang

et al. 2011

Mol Med Report

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Abstract. Neuropilin-1 (NRP-1) is a non-tyrosine kinase receptor for vascular endothelial growth factor (VEGF) that was recently found to play a role in tumor functions. Previous studies demonstrated that NRP-1 was overexpressed in a number of human tumors, including glioblastoma (GBM). However, the role of NRP-1 in glioma progression has yet to be adequately elucidated. Thus, we examined the expression of NRP-1 in human glioma cell lines using Western blotting, and cell cycle distribution and proliferation by transfection of the U373 cell line with NRP-1 short interference RNA (siRNA). Results showed NRP-1 siRNA to significantly reduce NRP-1 gene expression, decrease in vitro cell proliferation and induce cell apoptosis in cultured glioma cells, along with the accumulation of cells in the G1 phase and a decrease in cells in the S phase. Our results further revealed that NRP-1 knockdown decreased the expression levels of Bcl-2 family proteins and deactivated extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) signaling pathways, closely associated with cancer progression. Thus, our results provide a molecular mechanism for the effect of NRP-1 in tumors, rendering NRP-1 an attractive candidate as a therapeutic target in certain types of cancer, such as GBM.

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Role of recombinant mitogen-activated protein kinases JNK and p38 in the regulation of apoptosis in blood mononuclear cells under conditions of oxidative stress in vitro

Cited by 7 publications

References 8 publications

Apoptosis: Activation and Inhibition in Health and Disease

Apoptosis: Activation and Inhibition in Health and Disease

2‐Alkylsulfanyl‐4(5)‐aryl‐5(4)‐heteroarylimidazoles: An Overview on Synthetic Strategies and Biological Activity

RNA interference targeting NRP-1 inhibits human glioma cell proliferation and enhances cell apoptosis

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