2019
DOI: 10.1038/s41418-019-0456-9
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Ecdysone controlled cell and tissue deletion

Abstract: The removal of superfluous and unwanted cells is a critical part of animal development. In insects the steroid hormone ecdysone, the focus of this review, is an essential regulator of developmental transitions, including molting and metamorphosis. Like other steroid hormones, ecdysone works via nuclear hormone receptors to direct spatial and temporal regulation of gene transcription including genes required for cell death. During insect metamorphosis, pulses of ecdysone orchestrate the deletion of obsolete lar… Show more

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Cited by 50 publications
(56 citation statements)
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References 159 publications
(222 reference statements)
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“…However, in the case of an impaired immune response (second phase), virus will spread and massive destruction of the affected tissues will occur, followed by an induced innate inflammation in lungs mediated by pro-inflammatory macrophages, granulocytes, generation of pro-inflammatory cytokines and chemokines such as IL-6 and IP-10, macrophage inflammatory protein 1 such as MIP1α, MIP1β and MCP1. These inflammatory molecules attract monocytes, macrophages and T cells to the site of infection, promoting further inflammation creating overproduction of pro-inflammatory cytokines, which ultimately damage the lung structure and then the resulting cytokine storm enters the circulation system and reaches other organs, leading to a multi-organ damage [ 4 , 6 , 7 ]. Actually, data indicated that activation of the nuclear factor (NF)-κB transcription factor (NF-κB) signaling pathway represents a major contribution to the inflammation induced post SARS-CoV infection and that NF-κB inhibitors are promising antiviral drugs against infections caused by the virus and potentially other pathogenic human coronaviruses [ 8 ].…”
Section: Introductionmentioning
confidence: 99%
“…However, in the case of an impaired immune response (second phase), virus will spread and massive destruction of the affected tissues will occur, followed by an induced innate inflammation in lungs mediated by pro-inflammatory macrophages, granulocytes, generation of pro-inflammatory cytokines and chemokines such as IL-6 and IP-10, macrophage inflammatory protein 1 such as MIP1α, MIP1β and MCP1. These inflammatory molecules attract monocytes, macrophages and T cells to the site of infection, promoting further inflammation creating overproduction of pro-inflammatory cytokines, which ultimately damage the lung structure and then the resulting cytokine storm enters the circulation system and reaches other organs, leading to a multi-organ damage [ 4 , 6 , 7 ]. Actually, data indicated that activation of the nuclear factor (NF)-κB transcription factor (NF-κB) signaling pathway represents a major contribution to the inflammation induced post SARS-CoV infection and that NF-κB inhibitors are promising antiviral drugs against infections caused by the virus and potentially other pathogenic human coronaviruses [ 8 ].…”
Section: Introductionmentioning
confidence: 99%
“…Notably, our previous findings revealed that HP1γ, a reader protein of methylated histone H3 lysine 9 (H3K9me) [ 14 ], can recover the p53 protein expression levels through the epigenetic silencing of UBE2L3 [ 12 ]. We also found that HPV E6 expression leads to abnormal nuclear export of HP1γ, which contributes to excessive ubiquitination of p53 by UBE2L3 [ 15 ]. Thus, we strived to identify a way to overcome cisplatin resistance by utilizing HP1γ-mediated p53 stability.…”
Section: Introductionmentioning
confidence: 99%
“…SARS-CoV-2 is one of the most potent viruses to initiate the sepsis cascade and to induce pulmonary lesions with the development of ARDS ( Lin et al, 2018 ; Shi et al, 2020a ). The upregulation of pro-inflammatory cytokines and especially of IL-6 was observed in all severe forms, correlated with the incidence of the plasma viral load ( Chen et al, 2020 ) or other endogenic factors such as diabetes, cardiovascular disease or their associated treatments ( Qu et al, 2014 ).…”
Section: Sars-cov-2 Experimental Drugsmentioning
confidence: 99%