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Related Concept Videos

Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Apoptosis01:30

Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Negative Regulator Molecules01:23

Negative Regulator Molecules

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.

Alexandra N Brown-Suedel1,2, Lisa Bouchier-Hayes1,2

  • 1Hematology-Oncology Section, Department of Pediatrics, Department of Molecular Cell Biology, Baylor College of Medicine, Houston, TX, United States.

Frontiers in Cell and Developmental Biology
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PubMed
Summary

Caspase-2, a tumor suppressor protein, has unclear functions in apoptosis and cell cycle regulation. This review explores its substrates to understand its tumor-suppressing mechanism.

Keywords:
BIDMDM2PIDDRaiddapoptosiscaspase-2cell cycletumor suppressor

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Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Cancer Research

Background:

  • Caspase-2 is a member of the caspase protein family involved in apoptosis and inflammation.
  • It is recognized as a tumor suppressor, but its precise regulatory mechanisms remain largely unknown.
  • Conflicting evidence exists regarding its role in apoptosis, leading to its classification as an "orphan" caspase.

Purpose of the Study:

  • To review the known substrates of caspase-2.
  • To elucidate the functional relevance of these substrates to caspase-2's tumor suppressor activity.
  • To clarify the opposing functions of caspase-2 in apoptosis, cell cycle, and genomic stability.

Main Methods:

  • Literature review of existing studies on caspase-2.
  • Analysis of reported caspase-2 substrates.
  • Functional analysis of substrates in relation to tumor suppression.

Main Results:

  • Caspase-2 exhibits both apoptotic and non-apoptotic functions, including roles in cell cycle regulation and genomic instability.
  • The proteolytic cleavage of specific cellular substrates by caspase-2 is proposed as its primary mechanism of action.
  • Identified substrates play critical roles in cellular processes relevant to tumor suppression.

Conclusions:

  • Caspase-2's tumor suppressor function is mediated through the proteolytic activity on its substrates.
  • Understanding these substrates is key to deciphering the complex, dual role of caspase-2 in cellular regulation.
  • Further research into caspase-2 substrates will illuminate its therapeutic potential in cancer.