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Nanomagnetic Actuation: Controlling Cell Behavior with Magnetic Nanoparticles
Published in Jeffrey N. Anker, O. Thompson Mefford, Biomedical Applications of Magnetic Particles, 2020
The most extensively characterised modules of the MAPK family are ERK1/2, JNK, and p38. Each module is activated by numerous different extracellular cues but in general mitogenic and developmental stimuli preferentially activate ERK1/2, whereas JNK and p38 are more responsive to stress stimuli (Roux and Blenis 2004). Each family of the MAPK pathway is composed of a set of three conserved sequentially activated kinases each becoming phosphorylated in a cascade effect, triggered in response to extracellular signals.
Herbs in Cancer Therapy
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
Annum Malik, Shahzadi Sidra Saleem, Kifayat Ullah Shah, Learn-Han Lee, Bey Hing Goh, Tahir Mehmood Khan
In new clinical procedures, emphasis is laid on the blocking of specific cell signaling transduction pathways involved in converting normal cells into cancerous cells. Herbal drugs play their anticancerous role by blocking some of these pathways as follows: Pathway involving the activation of activator protein-1 (AP-1) and NF-kB: Pathogenesis of various inflammatory diseases including cancer, diabetes, rheumatoid arthritis, and atherosclerosis depends upon the activation of the NF-kB activation pathway.NF-kB along with other transcription factors including AP-1 regulates genes which play their role in angiogenesis and aggressive growth leading to cancer (Hemalswarya and Doble 2006). Mountain ginseng extract has shown to inhibit the lungs cancer cell growth through attenuating cancerous cells proliferation and by inducing apoptosis which is resulted through the controlling of NF-kB signaling transduction pathway (Hwang et al. 2012).Signal transduction through PTK: Polypeptide growth factors includes platelet derived growth factor (PGDF). These binds to their specific receptors which are called tyrosine kinesis. This binding of peptide growth factors with their receptors results in increased signal transduction to cancerous cells. Overexpression has been reported of these growth factors and their associated tyrosine kinesis receptors (Hemalswarya and Doble 2006).MAPK pathway: Activation of mitogen activated protein kinase (MAPK) cause proliferation of the cells. Variety of tumors are owing to the dysregulation in this MAPK pathway. Therefore an effective chemotherapy involves targeting of this MAPK pathway (Hemalswarya and Doble 2006). Zengshenping (zsp) is applied because it increases Capase-3 expression thus inducing tumor cell apoptosis (Guan et al. 2012).Cyclooxygenase-2 (COX-2) pathway: Proliferation as well as angio-genesis, either can be inhibited or stopped by the inhibition of cyclooxygenase (COX), mainly COX-2. This inhibition results in termination of the prostaglandin (PG) cascade ultimately effecting the growth of cancerous cells (Cragg and Newman 2005).
Protective effects of natural compounds against paraquat-induced pulmonary toxicity: the role of the Nrf2/ARE signaling pathway
Published in International Journal of Environmental Health Research, 2023
Hasan Badibostan, Nastaran Eizadi-Mood, A. Wallace Hayes, Gholamreza Karimi
Xuebijing injection is a Chinese herbal medicine consisting of a mixture of Chuanxiong, Chishao, Danshen, and Honghua (Liu et al. 2014). PQ increased MAPK expression and stimulated the production of TNF-α and IL-1β in the lungs of rats (Liu et al. 2014). p38 Mitogen-activated protein kinases (MAPK) are key mediators of cellular stressors such as inflammatory cytokines. MAPK indirectly decreased the Nrf2 level (Liu et al. 2014). Liu et al. investigated the protective effect of Xuebijing in an animal model. Their findings suggested that this herbal mixture decreased IL-6, TNF-α, IL-1β, IL-10, and TGF-β1 levels in PQ-treated animals. Although the levels of Nrf2 and GSH were increased in the lungs, Xuebijing was reported to protect rats against PQ lung-induced toxicity through the down-regulation of MAPK (Liu et al. 2014).
Cadmium stress in plants: A critical review of the effects, mechanisms, and tolerance strategies
Published in Critical Reviews in Environmental Science and Technology, 2022
Taoufik El Rasafi, Abdallah Oukarroum, Abdelmajid Haddioui, Hocheol Song, Eilhann E. Kwon, Nanthi Bolan, Filip M. G. Tack, Abin Sebastian, M. N. V. Prasad, Jörg Rinklebe
Sensing the presence of Cd in the extracellular environment can also lead to the activation of the mitogen-activated protein kinase (MAPK) network (Ghosh & Roy, 2019). This cascade is reported to be involved in signaling mechanisms and plant tolerance to Cd exposure (Chmielowska-Bąk et al., 2014; Dalcorso et al., 2010). MAPKs are a group of protein kinases (MAPK, MAPK kinase [MAPKK], and MAPK kinase [MAPKKK]) believed to be activated by phosphorylation due to the production of ROS under Cd stress (Gallego et al., 2012; Jain et al., 2018; Jalmi et al., 2018; Jonak et al., 2004; Ya-Fen & Aarts, 2012). It has been shown that both ZmMPK3-1 and ZmMPK6-1 genes are activated in maize under Cd exposure via the production of ROS (Liu et al., 2019). Similarly, the accumulation of ROS in Arabidopsis treated with Cd causes the activation of MPK3 and MPK6 genes involved in signal transduction (Liu et al., 2010). A higher gene expression of MAPKK2 was found in the roots of Glycine max seedlings exposed to 25 mg Cd L−1 for 6 h (Chmielowska-Bąk et al., 2013). Moreover, regulation of MAPKs leads to the alteration of plant response to Cd stress (Jagodzik et al., 2018) by controlling various gene responses such as of WRKY33 (Sun et al., 2020; Teramoto & Gutkind, 2013).
Cadmium induces cytotoxicity in normal mouse renal MM55.K cells
Published in International Journal of Environmental Health Research, 2022
Ho Jeong Lee, Ju Hong Lee, Seon Min Lee, Na Hyun Kim, Yeon Gyu Moon, Tae Kil Tak, Moonjung Hyun, Jeong Doo Heo
The MAPK pathway plays an important role in regulating cell proliferation and apoptosis. We examined the phosphorylation of MAPKs through western blot analysis of the CdCl2-induced apoptotic MM55.K cells. CdCl2 caused significant phosphorylation JNK and p38 but demonstrated dephosphorylation of ERK at concentrations of 7.5 and 15 µM in MM55.K cells. These findings suggest that CdCl2 induced apoptosis in MM55.K cells by modulating the MAPK pathways (Figure 4(g,h)). To further confirm the role of JNK and p38 in CdCl2-induced apoptotic MM55.K cells. We conducted an inhibitory assay with SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor). CdCl2 induced cell cytotoxicity in MM55.K cells were partially recovered by pretreatment with JNK and p38 inhibitor as compared with CdCl2 treated cells (Supplement Figure 1).