Phosphorylation of a critical threonine residue in the activation loop, Thr-160, allowing substrates to access the active site of the CDK

TLS Online TPP Program

#Id: 10564

#Unit 4. Cell Communication and Cell Signaling

Phosphorylated MLKL form

oligomers that insert into the plasma membrane and form holes, allowing Ca2+ entry.

TLS Online TPP Program

#Id: 10565

#Unit 4. Cell Communication and Cell Signaling

Ca2+ influx causes the cell and its organelles to swell

and burst, releasing its contents into the extracellular space which trigger activation of immune-system cells

and cause tissue inflammation and damage

TLS Online TPP Program

#Id: 10566

#Unit 4. Cell Communication and Cell Signaling

TLS Online TPP Program

#Id: 10567

#Unit 4. Cell Communication and Cell Signaling

Inflammation due to necroptosis has been implicated in mediating major human inflammatory diseases: rheumatoid arthritis, inflammatory bowel disease,

amyotrophic lateral sclerosis, Alzheimer’s disease and progressive atherosclerotic lesions

TLS Online TPP Program

#Id: 1607

#Unit 4. Cell Communication and Cell Signaling

Toll protein surprisingly revealed that its cytoplasmic signaling domain was homologous to that of the vertebrate receptor for the cytokine IL-1 (IL-1R).

TLS Online TPP Program

#Id: 1608

#Unit 4. Cell Communication and Cell Signaling

Apoptotic cells attract phagocytes by releasing the lipid mediator lysophosphatidic acid, which functions as a chemoattractant.