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Oryza sativa) during arsenic toxicity amelioration by a potential microbial consortium
Published in Yong-Guan Zhu, Huaming Guo, Prosun Bhattacharya, Jochen Bundschuh, Arslan Ahmad, Ravi Naidu, Environmental Arsenic in a Changing World, 2019
S. Awasthi, R. Chauhan, S. Srivastava, R.D. Tripathi
The present study indicates a practical potential for microbial application as an intervention strategy in mitigating As toxicity and reducing As uptake and translocation in rice plants. Supplementation of P. putida and C. vulgaris with 50µM As(V) significantly alleviated As induced growth inhibition in rice seedlings (Fig. 1), improved photosynthetic and antioxidant machinery and significantly decreased rice As concentration. Many proteins were differentially induced in rice seedlings by P. putida and C. vulgaris under As stress. The differentially expressed proteins were mainly involved to regulate defense system, photosynthesis, detoxification, plant hormones and energy metabolism. Heat shock protein are also found to be accumulated, which were a class of functionally related proteins involved in repair and aid in the renaturation of stress-damaged proteins, and reestablish cellular homeostasis, protect cells against the damage of stress (Ahsan et al., 2009). This study also revealed the expression of IAP100 (Inhibitor of Apoptosis) in the presence of consortium under As stress; IAP100 has ability to regulate caspases and also influence ubiquitin (Ub)-dependent pathways that modulate innate immune signaling. In conclusion, results provide new insights about the proteins and mechanisms involved in microbial consortium mediated As toxicity amelioration in rice.
Engineered flies for regeneration studies
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
In Drosophila, many signaling pathways converge into one apoptotic program, in which inhibitors of apoptosis and activators interplay to balance the death/live fate of a cell (Bergmann and Steller 2010). Cells have commonly inhibited the apoptotic pathway by the action of the inhibitor of apoptosis (IAP) proteins. The IAPs directly bind to caspases through the baculovirus IAP repeat (BIR) domain, thereby inhibiting their activation (Salvesen and Duckett 2002). Drosophila IAP (Diap1) can be inhibited by the family of IAP antagonists Reaper (Rpr), Hid and Grim proteins, initially discovered in flies (Goyal et al. 2000). This family of Diap1 inhibitors contains IAP-binding motifs (IBM) that are required to bind the BIR domains and hamper the anti-apoptotic function of IAP, thereby releasing the caspases from Diap1 (Sandu et al. 2010). Therefore, inducible expression of these Diap1 antagonists, mostly Hid and Rpr, has become a convenient way to induce apoptosis.
In Silico Approach to Cancer Therapy
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
Dysregulation of the apoptotic programmed cell death pathway is another characteristic of cancer. Caspases are crucial for apoptosis activation. Caspase proteins are from the cysteine proteases family, which has essential roles in apoptosis. The inhibitors of apoptosis (IAP) can constrain caspases. Legewie et al. (2006) have developed a model based on the caspase-3 and caspase-9 inhibition by IAPs. This results in the generation of implicit positive feedback leading to bistability and irreversibility in caspase activation.
Molecular dynamics simulation study on the inhibitory mechanism of RIPK1 by 4,5-dihydropyrazole derivatives
Published in Molecular Physics, 2023
Yurou Zhang, Song Wang, Aimin Ren, Shanshan Guan, E Jingwen, Zhijian Luo, Zhijie Yang, Xinyue Zhang, Juan Du, Hao Zhang
The mortality rate of digestive system neoplasms has gradually increased over the past decade. There is evidence that the receptor-interacting serine/threonine protein kinase 1 (RIPK1) is tightly connected to several digestive system neoplasms, such as liver cancer, colon cancer, and pancreatic cancer [1–5]. In tumour cells, the cellular inhibitor of apoptosis protein 1/2 (cIAP1/2) mediates RIPK1 ubiquitination, inducing a conformational change in the ubiquitinated RIPK1, which binds to transforming growth factor-β-activated kinase 1 (TAK1) to produce effects that maintain tumour cell survival [6,7]. Additionally, RIPK1 can keep tumour cell activity by triggering Caspase-8-dependent necroptosis pathways and collaborating with other factors to promote necrosome production, resist apoptosis, and antagonise chemotherapeutic drugs [8–11]. As a result, the design and development of kinase inhibitors targeting RIPK1 are of greatly meaningful for cancer treatment.
L-asparaginase from Dickeya chrysanthemi: expression, purification and cytotoxicity assessment
Published in Preparative Biochemistry & Biotechnology, 2022
Hesham Saeed, Eman Elsawy, Manal Shalaby, Manal Abdel-Fattah, Asmaa Hemida, Ahmad Eldoksh, Farid Shokry Ataya, Hesham Nematalla, Mohamed Elkewedi, Nikolaos N. Labrou, Nefertiti El-Nikhely
To complement this study, the levels of gene expression of Bax, survivin, and Ki-67 were determined using quantitative real time PCR. Bax is one of the proapoptotic markers within the Bcl-2 family of proteins and was the first member of this family to be discovered.[35] Ki-67 is an antigen associated with nuclear proliferation, expressed during the growth and synthesis phases of the cell cycle (G1, S, G2, and M) but not during the resting phase (G0).[36] The human protein survivin is a member of the inhibitor of apoptosis protein family, and participates in many important processes, such as reproduction, apoptosis, the cell cycle, development, metabolism, cell communications, and angiogenesis.[37,38] Survivin is strongly upregulated in most cancer cell types, in which it promotes tumor growth, survival, and metastasis, as well as the production of new vascularization.[38] In chronic myeloid leukemia high levels of survival have been associated with the late stages of disease and therapy resistance.[38] The apoptotic markers Bax, Ki-67, and survivin were significantly downregulated in L-ASNase treated cells by 73.5%, 56.9%, and 83.5% respectively, compared with untreated control THP-1 cells (Figure 6D–F), suggesting that the rD. chrysanthemi L-ASNase affected the proliferation of the THP-1 cells, triggering cell cycle arrest and induced cell death.
The expression of microRNAs and exposure to environmental contaminants related to human health: a review
Published in International Journal of Environmental Health Research, 2022
Maria Rosaria Tumolo, Alessandra Panico, Antonella De Donno, Pierpaolo Mincarone, Carlo Giacomo Leo, Roberto Guarino, Francesco Bagordo, Francesca Serio, Adele Idolo, Tiziana Grassi, Saverio Sabina
The association between several metals and PAHs with miRNAs expression was analyzed in a case–control study involving 360 healthy male coke oven workers. The expression of many plasma miRNAs was found to be negatively associated with aluminum, antimony, Pb, and titanium, and positively associated with molybdenum and tin. This study demonstrated a relationship between some miRNAs and biomarkers for genetic damage and oxidative stress, such as micronuclei and 8-OH-dG (Deng et al. 2019). Among the analyzed miRNAs, some have important functions. Let-7b-5p can regulate the expression of genes deputated to DNA-repair (Spolverini et al. 2017) and it is involved in p53-regulated pro-apoptotic pathway and nucleotide excision repair pathway (Saleh et al. 2011; Encarnación et al. 2016). miR-126-3p plays a role in cancer-related processes, such as inflammatory responses (Zampetaki and Mayr 2012). Improper expression of miR-16-5p can negatively affect DNA repair mechanism influencing the expression of DNA damage-related proteins (Patel et al. 2017). Finally, miR-320b is known to be down-regulated in human cancers; its target is TP53 regulated inhibitor of apoptosis 1 (TRIAP1) through which may control apoptosis process (Li et al. 2016). These findings may suggest a potential linkage between the metal-PAH complex interactions and the early harmful effects on human health (Deng et al. 2019).