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Related Concept Videos

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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 spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
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Separation of Sister Chromatids

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At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
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Anaphase Promoting Complex00:50

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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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Allosteric Proteins-ATCase01:19

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Binding sites linkages can regulate a protein's function.  For example, enzyme activity is often regulated through a feedback mechanism where the end product of the biochemical process serves as an inhibitor.
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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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Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
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The Paracaspase MALT1.

Janna Hachmann1, Guy S Salvesen2

  • 1Program in Cell Death and Survival Networks, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA; Graduate School of Biomedical Sciences, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.

Biochimie
|September 20, 2015
PubMed
Summary
This summary is machine-generated.

The Mucosa-Associated Lymphoid Tissue 1 (MALT1) paracaspase is crucial for NF-κB signaling through scaffolding and protease functions. Recent studies reveal its enzymatic mechanisms, substrates, and role in receptor-mediated signaling pathways.

Keywords:
CaspaseMucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1)NF-κB signalingProtease

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Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Signaling

Background:

  • The paracaspase MALT1 (Mucosa-Associated Lymphoid Tissue 1) is a key regulator of NF-κB signaling.
  • Its function involves both scaffolding and proteolytic activities, essential for immune responses.
  • Understanding MALT1's precise roles is critical for deciphering immune cell activation.

Purpose of the Study:

  • To review recent advancements in understanding MALT1's enzymatic mechanism and substrate specificity.
  • To summarize findings from various mouse models, including knockout and catalytically dead variants.
  • To elucidate the role of MALT1 in NF-κB signaling downstream of diverse receptors.

Main Methods:

  • Literature review of recent scientific publications.
  • Analysis of data from knockout and catalytically dead MALT1 mouse models.
  • Integration of findings on MALT1's enzymatic activity, substrates, and signaling pathways.

Main Results:

  • MALT1 exhibits complex enzymatic activity and cleaves specific substrates crucial for NF-κB activation.
  • Different mouse models have illuminated MALT1's scaffolding and proteolytic functions in vivo.
  • MALT1 integrates signals from various receptors to modulate NF-κB pathway activation.

Conclusions:

  • MALT1's dual function is central to its role in NF-κB signaling.
  • Continued research on MALT1's mechanism and substrates will advance our understanding of immune regulation.
  • MALT1 represents a potential therapeutic target for immune-related disorders.