GPR17 signaling activation by CHBC agonist induced cell death via modulation of MAPK pathway in glioblastoma

Life Sciences ◽  
2022 ◽  
Vol 291 ◽  
pp. 120307
Author(s):  
Phung Nguyen ◽  
Phuong Doan ◽  
Akshaya Murugesan ◽  
Thiyagarajan Ramesh ◽  
Tatu Rimpilainen ◽  
...  
Keyword(s):  
Cell Death ◽  
Mapk Pathway ◽  
Signaling Activation

scholarly journals Yeast Nap1-Binding Protein Nbp2p Is Required for Mitotic Growth at High Temperatures and for Cell Wall Integrity

Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 517-529
Author(s):  
Kentaro Ohkuni ◽  
Asuko Okuda ◽  
Akihiko Kikuchi
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
High Temperature ◽  
High Temperatures ◽  
Hybrid System ◽  
Mapk Pathway ◽  
Binding Protein ◽  
Cell Wall Integrity ◽  
Calcofluor White ◽  
Two Hybrid

AbstractNbp2p is a Nap1-binding protein in Saccharomyces cerevisiae identified by its interaction with Nap1 by a two-hybrid system. NBP2 encodes a novel protein consisting of 236 amino acids with a Src homology 3 (SH3) domain. We showed that NBP2 functions to promote mitotic cell growth at high temperatures and cell wall integrity. Loss of Nbp2 results in cell death at high temperatures and in sensitivity to calcofluor white. Cell death at high temperature is thought not to be due to a weakened cell wall. Additionally, we have isolated several type-2C serine threonine protein phosphatases (PTCs) as multicopy suppressors and MAP kinase-kinase (MAPKK), related to the yeast PKC MAPK pathway, as deletion suppressors of the nbp2Δ mutant. Screening for deletion suppressors is a new genetic approach to identify and characterize additional proteins in the Nbp2-dependent pathway. Genetic analyses suggested that Ptc1, which interacts with Nbp2 by the two-hybrid system, acts downstream of Nbp2 and that cells lacking the function of Nbp2 prefer to lose Mkk1, but the PKC MAPK pathway itself is indispensable when Nbp2 is deleted at high temperature.

scholarly journals FLT3 tyrosine kinase inhibitors synergize with BCL-2 inhibition to eliminate FLT3/ITD acute leukemia cells through BIM activation

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Ruiqi Zhu ◽  
Li Li ◽  
Bao Nguyen ◽  
Jaesung Seo ◽  
Min Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Mapk Pathway ◽  
Selective Inhibitor ◽  
Leukemia Cells ◽  
Sorafenib Treatment ◽  
Limited Success ◽  
Pathway Inhibition

AbstractTyrosine kinase inhibitors (TKIs) targeting FLT3 have shown activity but when used alone have achieved limited success in clinical trials, suggesting the need for combination with other drugs. We investigated the combination of FLT3 TKIs (Gilteritinib or Sorafenib), with Venetoclax, a BCL-2 selective inhibitor (BCL-2i), on FLT3/ITD leukemia cells. The combination of a FLT3 TKI and a BCL-2i synergistically reduced cell proliferation and enhanced apoptosis/cell death in FLT3/ITD cell lines and primary AML samples. Venetoclax also re-sensitized FLT3 TKI-resistant cells to Gilteritinib or Sorafenib treatment, mediated through MAPK pathway inhibition. Gilteritinib treatment alone dissociated BIM from MCL-1 but increased the binding of BIM to BCL-2. Venetoclax treatment enhanced the binding of BIM to MCL-1 but dissociated BIM from BCL-2. Treatment with the drugs together resulted in dissociation of BIM from both BCL-2 and MCL-1, with an increased binding of BIM to the cell death mediator BAX, leading to increased apoptosis. These findings suggest that Venetoclax mitigates the unintended pro-survival effects of FLT3 TKI mainly through the dissociation of BIM and BCL-2 and also decreased BIM expression. This study provides evidence that the addition of BCL-2i enhances the effect of FLT3 TKI therapy in FLT3/ITD AML treatment.

scholarly journals Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1011-1022 ◽  
Author(s):  
T.L. Gumienny ◽  
E. Lambie ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
M.O. Hengartner
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Somatic Cell ◽  
Cell Fate ◽  
Germ Cells ◽  
Mapk Pathway ◽  
Apoptotic Cell ◽  
C Elegans ◽  
Pathway Activation

Development of the nematode Caenorhabditis elegans is highly reproducible and the fate of every somatic cell has been reported. We describe here a previously uncharacterized cell fate in C. elegans: we show that germ cells, which in hermaphrodites can differentiate into sperm and oocytes, also undergo apoptotic cell death. In adult hermaphrodites, over 300 germ cells die, using the same apoptotic execution machinery (ced-3, ced-4 and ced-9) as the previously described 131 somatic cell deaths. However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis. Germ cell death requires ras/MAPK pathway activation and is used to maintain germline homeostasis. We suggest that apoptosis eliminates excess germ cells that acted as nurse cells to provide cytoplasmic components to maturing oocytes.

scholarly journals Correction to: A novel coordination complex of platinum (PT) induces cell death in colorectal cancer by altering redox balance and modulating MAPK pathway

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Khayal Al-Khayal ◽  
Mansoor-Ali Vaali-Mohammed ◽  
Mohammed Elwatidy ◽  
Thamer Bin Traiki ◽  
Omar Al-Obeed ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Mapk Pathway ◽  
Redox Balance ◽  
Coordination Complex

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals Notch signaling activation induces cell death in MAPKi‐resistant melanoma cells

2019 ◽  
Vol 32 (4) ◽  
pp. 528-539 ◽  
Author(s):  
Dareen M. Mikheil ◽  
Kirthana Prabhakar ◽  
Ayyan Arshad ◽  
Carlos I. Rodriguez ◽  
Michael A. Newton ◽  
...  
Keyword(s):  
Cell Death ◽  
Notch Signaling ◽  
Melanoma Cells ◽  
Signaling Activation

Inhibition of the Cardiac p38-MAPK Pathway by SB203580 Delays Ischemic Cell Death

2000 ◽  
Vol 35 (3) ◽  
pp. 474-483 ◽  
Author(s):  
Miroslav Barancik ◽  
Patrik Htun ◽  
Claudia Strohm ◽  
Sven Kilian ◽  
Wolfgang Schaper
Keyword(s):  
Cell Death ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
P38 Mapk Pathway
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