scholarly journals Bisphenol A exposure triggers apoptosis via three signaling pathways in Caenorhabditis elegans

RSC Advances ◽  
2017 ◽  
Vol 7 (52) ◽  
pp. 32624-32631 ◽  
Author(s):  
Yun Wang ◽  
Lianfeng Zhang ◽  
Xun Luo ◽  
Shunchang Wang ◽  
Yuanyuan Wang
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Growth Factor ◽  
Bisphenol A ◽  
Signaling Pathways ◽  
Dna Damage Response ◽  
Mitogen Activated Protein Kinase ◽  
Mapk Cascades ◽  
Damage Response ◽  
Mitogen Activated Protein

Bisphenol A can trigger germline apoptosis via three signaling pathways including DNA damage response (DDR) pathway, mitogen-activated protein kinase (MAPK) cascades and insulin-like growth factor-1 (IGF-1) network in Caenorhabditis elegans.

scholarly journals Avian Sarcoma and Leukosis Virus Cytopathic Effect in the Absence of TVB Death Domain Signaling

2005 ◽  
Vol 79 (13) ◽  
pp. 8243-8248 ◽  
Author(s):  
Sara Klucking ◽  
Asha S. Collins ◽  
John A. T. Young
Keyword(s):  
Dna Damage ◽  
Signaling Pathways ◽  
Dna Damage Response ◽  
Cytopathic Effect ◽  
Tumor Necrosis Factor Receptor ◽  
Death Domain ◽  
Trail Receptors ◽  
Damage Response ◽  
Cellular Dna ◽  
Avian Sarcoma

ABSTRACT The cytopathic effect (CPE) seen with some subgroups of avian sarcoma and leukosis virus (ASLV) is associated with viral Env activation of the death-promoting activity of TVB (a tumor necrosis factor receptor-related receptor that is most closely related to mammalian TNF-related apoptosis-inducing ligand [TRAIL] receptors) and with viral superinfection leading to unintegrated viral DNA (UVD) accumulation, which is presumed to activate a cellular DNA damage response. In this study, we employed cells that express signaling-deficient ASLV receptors to demonstrate that an ASLV CPE can be uncoupled from the death-promoting functions of the TVB receptor. However, these cell-killing events were associated with much higher levels of viral superinfection and DNA accumulation than those seen when the virus used signaling-competent TVB receptors. These findings suggest that a putative cellular DNA damage response that is activated by UVD accumulation might act in concert with the death-signaling pathways activated by Env-TVB interactions to trigger cell death. Such a model is consistent with the well-established synergy that exists between TRAIL-signaling pathways and DNA damage responses which is currently being exploited in cancer therapy regimens.

scholarly journals Interactions of ErbB4 and Kap1 Connect the Growth Factor and DNA Damage Response Pathways

2010 ◽  
Vol 8 (10) ◽  
pp. 1388-1398 ◽  
Author(s):  
Maureen Gilmore-Hebert ◽  
Rajani Ramabhadran ◽  
David F. Stern
Keyword(s):  
Dna Damage ◽  
Growth Factor ◽  
Dna Damage Response ◽  
Damage Response

scholarly journals A simple answer to complex questions: Caenorhabditis elegans as an experimental model for examining the DNA damage response and disease genes

2017 ◽  
Vol 233 (4) ◽  
pp. 2781-2790 ◽  
Author(s):  
Matthias Rieckher ◽  
Arturo Bujarrabal ◽  
Markus A. Doll ◽  
Najmeh Soltanmohammadi ◽  
Björn Schumacher
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Experimental Model ◽  
Dna Damage Response ◽  
Disease Genes ◽  
Damage Response

Nerve growth factor functions as a chemoattractant for mast cells through both mitogen-activated protein kinase and phosphatidylinositol 3-kinase signaling pathways

Blood ◽  
2000 ◽  
Vol 95 (6) ◽  
pp. 2052-2058 ◽  
Author(s):  
Junko Sawada ◽  
Atsuko Itakura ◽  
Akane Tanaka ◽  
Tohru Furusaka ◽  
Hiroshi Matsuda
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Mast Cells ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
Mitogen Activated Protein Kinase ◽  
Phosphatidylinositol 3 Kinase ◽  
Directional Migration ◽  
Nerve Growth ◽  
Mitogen Activated Protein

Abstract Despite being a well-characterized neurotrophic factor, nerve growth factor (NGF) influences survival, differentiation, and functions of mast cells. We investigated whether NGF was able to induce directional migration of rat peritoneal mast cells (PMCs). NGF clearly induced chemotactic movement of PMCs in a dose-dependent manner with the drastic morphological change and distribution of F-actin, which was completely blocked by pretreatment with Clostridium botulinumC2 toxin, an actin-polymerization inhibitor. Because PMCs constitutively express the NGF high-affinity receptor (TrkA) with a tyrosine kinase domain, we focused on downstream effectors in signaling cascades following the TrkA. NGF rapidly activated both mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K), and the addition of inhibitors specific for MAPK kinase and PI3K suppressed cell migration and these signals. In the coculture system with PMCs and fibroblasts, which produce biologically active NGF, directional migration of PMCs to fibroblasts was observed, and the addition of anti-NGF polyclonal antibodies significantly suppressed the migration of PMCs. These findings suggested that NGF initiated chemotactic movement of PMCs through both MAPK and PI3K signaling pathways following TrkA activation. Thus, locally produced NGF may play an important role in mast cell accumulation in allergic and nonallergic inflammatory conditions.

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