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Your search keyword '"Kannan, Rajaretinam Rajesh"' showing total 5 results
Start Over Author "Kannan, Rajaretinam Rajesh" Publisher elsevier
5 results on '"Kannan, Rajaretinam Rajesh"'

2. List of contributors

Author

Ajit, Shilpa, primary, Amrutha, C., additional, Anju, M.S., additional, Anupama Sekar, J., additional, Arshajyothirmayi, V.A., additional, Ashok, Arathi, additional, Aswathy, M.R., additional, Athira, R.K., additional, Bartwal, Gaurav, additional, Bhatt, Anugya, additional, Borah, Ankita, additional, Chakraborty, Monalisa, additional, Chakraborty, Saptomee, additional, Chauhan, Neha, additional, Das, Apurba, additional, Das, Sreyashi, additional, Freeman, Jennifer L., additional, G, Gayathry, additional, Garg, Akansha, additional, Geeverghese, Rency, additional, Gulia, Kamalesh K., additional, Harikrishnan, V.S., additional, Joshi, S.R., additional, Kannan, Rajaretinam Rajesh, additional, Kasoju, Naresh, additional, Kaur, Tejinder, additional, Komath, Manoj, additional, Komeri, Remya, additional, Kripamol, R., additional, Kumar, D. Sakthi, additional, Kumar, Pramod, additional, Maya, B., additional, Misra, Santosh K., additional, Murkunde, Yogeshkumar, additional, Nagesh, D.S., additional, Naik, Aishwarya, additional, Nandi, Moumita, additional, Nayar, Seema A., additional, P, Lekshmi, additional, P Nair, Renjith, additional, P.R., Anil Kumar, additional, Mohanan, P.V., additional, Pai, Roopesh R., additional, Pakshirajan, Kannan, additional, Pant, A.B., additional, Paul, Tanushree, additional, Pitchai, Arjun, additional, Pugazhenthi, G., additional, Pun, Bishal, additional, R, Rashmi, additional, Raju, Riya, additional, Ramasamy, Surjith, additional, Rao, Alka, additional, Rathee, Garima, additional, Rathee, Jyotsna, additional, Remya, N.S., additional, Saha, Triya, additional, Sangeetha, V.P., additional, Santhakumar, Syama, additional, Shah, Lekha, additional, Shankar, Pramod, additional, Singh, Kuljit, additional, Singh, Manvi, additional, Singh, S., additional, Solanki, Pratima R., additional, Thomas, Lynda Velutheril, additional, Tirella, Annalisa, additional, Velayudhan, Shiny, additional, Venugopal, Akhil, additional, Vinodkumar, V., additional, and Xavier, Joseph, additional

Published
2022
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4. Contributors

Author

Abbas, Shah Rukh, primary, Aftab, Ayesha, additional, Ahmed, Shanzay, additional, Amri, Hakima, additional, Bakhtiar, Syeda Marriam, additional, Bashir, Iqra, additional, Bhatti, Attya, additional, Buriani, Alessandro, additional, Butt, Hina Aslam, additional, Carrara, Maria, additional, Chakravorty, Kamaljyoti, additional, Chen, Yong, additional, Court, Colin M., additional, Dhawan, Dipali, additional, DiPardo, Benjamin, additional, Dwivedi, Shailendra, additional, Fayyaz, Syeda Maham, additional, Fortinguerra, Stefano, additional, Fu, Li-Wu, additional, Gabbia, Daniela, additional, Hashmi, Muhammad Uzair, additional, Izci, Yusuf, additional, John, Peter, additional, Kalia, Anu, additional, Kambale, Rohit, additional, Kaneko, Satoru, additional, Kannan, Rajaretinam Rajesh, additional, Kaur, Raman Preet, additional, Khan, Muhammad Qasim, additional, Khurshid, Sobia, additional, Liang, Shao-Bo, additional, Lingeswaran, Malavika, additional, Ludhiadch, Abhilash, additional, Misra, Radhieka, additional, Misra, Sanjeev, additional, Munir, Anum, additional, Munshi, Anjana, additional, Muthurajan, Raveendran, additional, Nadeem, Mohammad, additional, Nalbantoglu, Sinem, additional, Pareek, Puneet, additional, Purohit, Purvi, additional, Qayyum, Hajra, additional, Rahman, Hifzur, additional, Saghir, Yumna, additional, Sharma, Praveen, additional, Sharma, Sat Pal, additional, Sho, Shonan, additional, Siddiqui, Mohammed Haris, additional, Soomro, Naveed Iqbal, additional, Soomro, Saeed Iqbal, additional, Sorrenti, Vincenzo, additional, Srinivasan, Thanga Suja, additional, Syed, Nida Ali, additional, Syed, Huma, additional, Takamatsu, Kiyoshi, additional, Talukdar, Dibyendu, additional, Tomlinson, James S., additional, Vishnoi, Jeewan Ram, additional, and Winograd, Paul, additional

Published
2019
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5. Bisphenol-A alters hematopoiesis through EGFR/ERK signaling to induce myeloblastic condition in zebrafish model.

Author

Sundarraj S, Sujitha MV, Alphonse CRW, Kalaiarasan R, and Kannan RR

Subjects
Animals, Benzhydryl Compounds toxicity, ErbB Receptors, Hematopoiesis, Larva, Granulocyte Precursor Cells, Zebrafish
Abstract

Experimental evidence from the etiology of cancer studies suggests that a correlation between Bisphenol-A (BPA) exposure and alterations in hematopoiesis leads to blood cancer. In our study zebrafish were used to assess the lethality, developmental effect, embryonic apoptosis and changes in transcription factor of hematopoiesis through EGFR/ERK signaling pathways in response to BPA. The in silico interaction of EGFR and BPA was analysed by molecular dynamic simulation. According to our results, BPA induced a significant lethal effect in hatching retardation, reduction in heart rate and teratogenic effects on zebrafish embryos and larvae at three different concentrations 100, 500 and 2500 μg/L. The mortality of adult zebrafish exposed to the acute toxicity of BPA from 5 to 30 mg/L concentrations was determined for 96 h. The peripheral blood cells and vital organs such as kidney, liver and spleen from BPA exposed fish showed predominantly abnormal myeloid blast cells along with severe morphological changes in erythrocytes at sublethal concentration 245 μg/L. The BPA showed the highest binding affinity to zebrafish EGFR with a docking score of -7.5 kcal/mol with an RMSD of 3.0 nm during MD simulation. We found that EGFR/ERK overexpression leads to induce hematopoietic cell proliferation and impaired differentiation, which enhances the myeloid repopulating activity and the accumulation of immature myeloblast cells. BPA also caused a corresponding increase in expression of hematopoietic transcription factor c-MYB and RUNX-1 leading to polychromasia, poikilocytosis, acanthocytes and anisocytosis and promoted myeloblastosis by inhibiting GATA-1 expression. These morphological changes often resulted in the prior condition of acute myeloid leukemia (AML). Comprehensively, our data suggest that BPA can trigger the malignancy of AML cells by alteration of respective hematopoietic transcription factors via EGFR/ERK signaling in the zebrafish model., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Published
2021
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