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Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

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Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
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Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Complementation Tests00:49

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A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
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MAPK Signaling Cascades01:07

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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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Updated: Jan 20, 2026

Real-Time Monitoring and Modulation of Blood Pressure in a Rabbit Model of Ischemic Stroke
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Therapeutic Modulation of the Complement Cascade in Stroke.

Alison R Clarke1, Brandon R Christophe1, Anadjeet Khahera1

  • 1Cerebrovascular Research Laboratory, Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY, United States.

Frontiers in Immunology
|August 17, 2019
PubMed
Summary
This summary is machine-generated.

Complement cascade blockade early after ischemic stroke improves outcomes, but inhibiting it during recovery may be harmful. Targeted therapies are needed for successful clinical translation.

Keywords:
cerebral blood flowcomplementcomplement activationcomplement cascadestroke therapyvascular disorders

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Area of Science:

  • Neuroscience
  • Immunology
  • Cardiovascular Medicine

Background:

  • Stroke is a major cause of death and disability globally.
  • Ischemic stroke patients often receive reperfusion therapies.
  • The complement cascade is implicated in secondary injury following reperfusion.

Purpose of the Study:

  • To investigate the role of the complement cascade in ischemic stroke.
  • To evaluate the therapeutic potential of complement blockade at different stages of stroke recovery.

Main Methods:

  • Review of human and experimental models of reperfused ischemic stroke.
  • Analysis of data implicating complement pathways (lectin and alternative) and effectors (C3a, C5a).
  • Assessment of outcomes following acute versus delayed complement cascade blockade.

Main Results:

  • Early complement cascade blockade during thrombolysis improves tissue survival and functional outcomes.
  • Blocking the complement cascade during the repair and recovery phase is detrimental.
  • Emerging data suggest delayed complement pathway upregulation may aid recovery.

Conclusions:

  • Acute complement cascade inhibition is a promising therapeutic strategy for ischemic stroke.
  • Timing of complement blockade is critical; early intervention is beneficial, while late intervention is harmful.
  • Future strategies must target early effectors without impeding delayed repair processes for successful clinical translation.