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Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
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Signal Transduction: Overview01:26

Signal Transduction: Overview

Cells respond to many types of information, often through receptor proteins positioned on the membrane. They respond to chemical signals, such as hormones, neurotransmitters, and other signaling molecules, initiating a series of molecular reactions to produce an appropriate response. This is called signal transduction. Cells also coordinate different responses elicited by the same signaling molecule via mediators, allowing molecular cross-talk.
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Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...
Diversity in Cell Signaling Responses01:22

Diversity in Cell Signaling Responses

The physiological function of a cell and cellular communication are outcomes of a range of extrinsic signals, intracellular signaling pathways, and cellular responses. No two cell types express the same repertoire of signaling components. Receptors are highly selective for their cognate ligands, but once activated, they can alter multiple cellular processes such as DNA transcription, protein synthesis, and metabolic activity. 
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Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

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...
Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

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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Critical signal transduction pathways in CLL.

Asish K Ghosh1, Neil E Kay

  • 1Division of Hematology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA.

Advances in Experimental Medicine and Biology
|September 10, 2013
PubMed
Summary

Aberrant signaling from receptor tyrosine kinases (RTKs) and non-RTKs promotes survival and therapy resistance in chronic lymphocytic leukemia (CLL) B cells. Targeting these aberrant kinases offers potential new therapeutic strategies for CLL.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Receptor tyrosine kinases (RTKs) are crucial for signal transduction in normal and malignant cells.
  • Constitutively active RTKs and non-RTKs contribute to leukemic cell survival and chemoresistance in chronic lymphocytic leukemia (CLL).
  • CLL B cells may activate RTKs via autocrine cytokine loops.

Purpose of the Study:

  • To review the impact of aberrant RTK and non-RTK activity on CLL B cell survival.
  • To explore the potential of targeting these signaling pathways for novel CLL therapies.

Main Methods:

  • Literature review of aberrant RTK and non-RTK signaling in CLL.
  • Analysis of mechanisms contributing to CLL B cell survival and therapy resistance.
  • Evaluation of potential therapeutic targets within these signaling pathways.

Main Results:

  • Constitutive activation of multiple RTKs enhances CLL B cell survival and resistance to apoptosis.
  • Aberrant expression and activation of non-RTKs, such as Src/Syk kinases, also confer therapy resistance.
  • Autocrine cytokine loops may contribute to sustained RTK activation in CLL B cells.

Conclusions:

  • Aberrant RTK and non-RTK signaling pathways are key drivers of CLL pathogenesis.
  • Targeting these aberrant kinases represents a promising therapeutic strategy for chronic lymphocytic leukemia.
  • Further research into these signaling components could lead to improved CLL treatment outcomes.