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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Cellular functions of programmed cell death 5.

Ge Li1, Dalong Ma1, Yingyu Chen1

  • 1Department of Immunology, Peking University School of Basic Medical Sciences, 38 Xueyuan Road, Beijing 100191, China; Center for Human Disease Genomics, Peking University, 38 Xueyuan Road, Beijing 100191, China.

Biochimica Et Biophysica Acta
|January 19, 2016
PubMed
Summary
This summary is machine-generated.

Programmed cell death 5 (PDCD5) is a key protein regulating apoptosis and immune responses. Its nuclear translocation and interactions with transcription factors are crucial for cellular functions and are often disrupted in cancer.

Keywords:
ApoptosisAutoimmune diseasesImmune regulationPDCD5Programmed cell death 5Tumor

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Programmed cell death 5 (PDCD5) is an evolutionarily conserved protein.
  • PDCD5 plays critical roles in programmed cell death and immune regulation.
  • Its functions are linked to signaling networks frequently altered in cancer cells.

Purpose of the Study:

  • To review the known cellular functions of Programmed cell death 5 (PDCD5).
  • To highlight PDCD5's role in apoptosis acceleration and immune regulation.
  • To discuss the molecular mechanisms and regulatory pathways involving PDCD5.

Main Methods:

  • Literature review of studies on PDCD5.
  • Analysis of PDCD5's interactions with key proteins like TIP60, HDAC3, MDM2, and TP53.
  • Examination of PDCD5's role in regulatory T cell function via the PDCD5-TIP60-FOXP3 pathway.

Main Results:

  • PDCD5 accelerates apoptosis across various cell types and stimuli.
  • PDCD5 translocates to the nucleus, regulating transcription factors involved in cancer.
  • PDCD5 promotes regulatory T cell function through the PDCD5-TIP60-FOXP3 pathway.
  • PDCD5 stability is modulated by proteins including NF-κB p65, OTUD5, YAF2, and DNAJB1.
  • Phosphorylation at Ser119 by CK2 is essential for PDCD5 nuclear translocation under genotoxic stress.

Conclusions:

  • PDCD5 is a multifunctional protein with significant roles in cell death and immunity.
  • Dysregulation of PDCD5-associated signaling pathways contributes to cancer development.
  • Understanding PDCD5's mechanisms offers potential therapeutic insights for cancer and immune disorders.