scholarly journals Programmed Cell Death in Cortical Chick Embryo Astrocytes Is Associated with Activation of Protein Kinase PK60 and Ceramide Formation

2002 ◽  
Vol 70 (1) ◽  
pp. 130-138 ◽  
Author(s):  
Dimitra Mangoura ◽  
Glyn Dawson
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Chick Embryo ◽  
Programmed Cell Death

scholarly journals Regulation of programmed cell death during neural induction in the chick embryo

2011 ◽  
Vol 55 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Anna Gibson ◽  
Neil Robinson ◽  
Andrea Streit ◽  
Guojun Sheng ◽  
Claudio D. Stern
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Programmed Cell Death ◽  
Neural Induction

scholarly journals RIPK1 Is Cleaved by 3C Protease of Rhinovirus A and B Strains and Minor and Major Groups

Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2402
Author(s):  
Sarah N. Croft ◽  
Erin J. Walker ◽  
Reena Ghildyal
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Protease Inhibitor ◽  
Phylogenetic Groups ◽  
Viral Protease ◽  
Interacting Protein ◽  
3C Protease ◽  
Survival Pathways ◽  
Integral Role

Rhinoviruses (RV), like many other viruses, modulate programmed cell death to their own advantage. The viral protease, 3C has an integral role in the modulation, and we have shown that RVA-16 3C protease cleaves Receptor-interacting protein kinase-1 (RIPK1), a key host factor that modulates various cell death and cell survival pathways. In the current study, we have investigated whether this cleavage is conserved across selected RV strains. RIPK1 was cleaved in cells infected with strains representing diversity across phylogenetic groups (A and B) and receptor usage (major and minor groups). The cleavage was abrogated in the presence of the specific 3C protease inhibitor, Rupintrivir. Interestingly, there appears to be involvement of another protease (maybe 2A protease) in RIPK1 cleavage in strains belonging to genotype B. Our data show that 3C protease from diverse RV strains cleaves RIPK1, highlighting the importance of the cleavage to the RV lifecycle.

scholarly journals Death-associated protein kinase (DAPK) and signal transduction: blebbing in programmed cell death

FEBS Journal ◽  
2009 ◽  
Vol 277 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Miia Bovellan ◽  
Marco Fritzsche ◽  
Craig Stevens ◽  
Guillaume Charras
Keyword(s):  
Signal Transduction ◽  
Cell Death ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Death Associated Protein Kinase

scholarly journals Regulation of programmed cell death ligand 1 expression by atypical protein kinase C lambda/iota in cutaneous angiosarcoma

2019 ◽  
Vol 110 (5) ◽  
pp. 1780-1789 ◽  
Author(s):  
Ai Kawamura ◽  
Takuji Kawamura ◽  
Meghan Riddell ◽  
Takao Hikita ◽  
Teruki Yanagi ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Atypical Protein Kinase C ◽  
Atypical Protein Kinase ◽  
Kinase C

La morphogenèse du pied de l'embryon de poulet étudiée à l'aide de malformations provoquées par le vert Janus

Development ◽  
1976 ◽  
Vol 35 (3) ◽  
pp. 649-665
Author(s):  
Marie-Paule Pautou
Keyword(s):  
Cell Death ◽  
Single Dose ◽  
Soft Tissue ◽  
Chick Embryo ◽  
Programmed Cell Death ◽  
Apical Growth ◽  
Chick Embryos ◽  
Janus Green

Morphogenesis of the chick embryo foot as studied by Janus green B-induced malformations Janus green was injected into the amnioticsac of 6·5-day-old chick embryos at a single dose of 8·5 or 15 μg; the dye causes respectively 55 and 82 % malformations of the feet. Toes are affected by partial or total soft tissue syndactyly, hypophalangy and infrequently by hyperphalangy. Lateral toes are more severely and more frequently affected by syndactyly and hypophalangy than medium ones. Hyperphalangy is found exclusively in toes I and II and causes the formation of one excess phalanx at most Syndactylous toes are joined by an overdeveloped digital membrane. Hypophalangic toes have a truncated (non-pointed) distaltip. Two phalanges are lacking at most. These malformations are due to two distinct phases of the Janus green action. The first one, which is early and fast, inhibits interdigital programmed cell death, causing in term the non-regression of the inter digital membranes and thus syndactyly. The second one, which is late and slow, blocks the apical growth; this leads to hypophalangy.

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