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Notch Signaling Pathway

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...

Notch Signaling Pathway

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...

Assembly of Signaling Complexes

Assembly of Signaling Complexes

Multiprotein signaling complexes are formed in a dynamic process involving protein-protein interactions at the cytoplasmic domain of transmembrane receptors or enzymatic and non-enzymatic proteins associated with the receptor. These complexes ensure the activation and propagation of intracellular signals that regulate cell functions.
Interaction domains in cell signaling
Interaction domains recognize exposed features of their binding partners containing post-translationally modified sequences,...

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

Hedgehog Signaling Pathway

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...

Hedgehog Signaling Pathway

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...

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Related Experiment Video

Updated: Jun 16, 2026

Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

P66Shc signals to age.

Mirella Trinei¹, Ina Berniakovich, Elena Beltrami

¹Congenia Srl, 20139 Milan, Italy.

|February 17, 2010

Summary

This summary is machine-generated.

Reactive oxygen species (ROS) impact aging. Research on p66Shc suggests ROS signaling, not just damage, influences aging and longevity, impacting degenerative diseases.

Keywords:

Aging Life span degenerative disease oxidative stress

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Published on: April 16, 2012

Techniques to Induce and Quantify Cellular Senescence

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

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Last Updated: Jun 16, 2026

Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Quantitative Imaging of Lineage-specific Toll-like Receptor-mediated Signaling in Monocytes and Dendritic Cells from Small Samples of Human Blood

Quantitative Imaging of Lineage-specific Toll-like Receptor-mediated Signaling in Monocytes and Dendritic Cells from Small Samples of Human Blood

Published on: April 16, 2012

Techniques to Induce and Quantify Cellular Senescence

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Area of Science:

Biochemistry
Molecular Biology
Gerontology

Background:

Oxygen metabolism generates reactive oxygen species (ROS), implicated in aging.
ROS are traditionally viewed as damaging agents contributing to cellular senescence.
p66Shc is a key regulator of intracellular ROS levels and aging processes.

Purpose of the Study:

To investigate the role of p66Shc in aging and ROS regulation.
To explore the signaling function of ROS beyond their damaging properties.
To determine how ROS signaling affects longevity and degenerative diseases.

Main Methods:

Studied the function of p66Shc in cellular and organismal aging.
Analyzed the impact of ROS levels regulated by p66Shc.
Investigated the correlation between ROS signaling pathways and aging phenotypes.

Main Results:

p66Shc plays a critical role in regulating ROS levels associated with aging.
Evidence suggests ROS exert specific signaling functions influencing aging.
These signaling functions appear distinct from the general damaging effects of ROS.

Conclusions:

The signaling capacity of ROS, modulated by p66Shc, is a key determinant of aging.
Longevity and the incidence of age-related degenerative diseases are influenced by ROS signaling.
This challenges the traditional view of ROS solely as damaging molecules in aging.