Figure 5
Regulation and dysregulation of TP53 function implicated in lymphomagenesis. (1) At the DNA level, dysregulation of transcription factors and hypermethylation can silence gene expression. (2) At the RNA level, posttranscriptional regulation events include alternative splicing that produces p53 isoforms with altered function, mRNA stability/degradation, and translational regulation. (3) At the protein level, posttranslational modification, redox regulation, and p53 regulators affect p53 stability and function in the nucleus and cytoplasm. (4) p53-independent pathways, including PI3K/Akt affects p53-dependent apoptotic pathway. (5) Autophagy caused by ER stress, starvation, and other forms of stress inhibits p53-dependent apoptosis in most cases. Conversely, cytoplasmic p53 inhibits autophagy by promoting the mTOR pathway, whereas nuclear p53 stimulates autophagy by transactivating genes involved in autophagy. MOMP indicates mitochondrial outer membrane permeabilization; and U or Ub, ubiquitination.

Regulation and dysregulation of TP53 function implicated in lymphomagenesis. (1) At the DNA level, dysregulation of transcription factors and hypermethylation can silence gene expression. (2) At the RNA level, posttranscriptional regulation events include alternative splicing that produces p53 isoforms with altered function, mRNA stability/degradation, and translational regulation. (3) At the protein level, posttranslational modification, redox regulation, and p53 regulators affect p53 stability and function in the nucleus and cytoplasm. (4) p53-independent pathways, including PI3K/Akt affects p53-dependent apoptotic pathway. (5) Autophagy caused by ER stress, starvation, and other forms of stress inhibits p53-dependent apoptosis in most cases. Conversely, cytoplasmic p53 inhibits autophagy by promoting the mTOR pathway, whereas nuclear p53 stimulates autophagy by transactivating genes involved in autophagy. MOMP indicates mitochondrial outer membrane permeabilization; and U or Ub, ubiquitination.

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