2016 Group Project 2: Difference between revisions
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===Introduction=== | ===Introduction=== | ||
The Notch signalling pathway is critical for cell differentiation, proliferation, and apoptosis. It is involved in embryonic organ development through the regulation of cell-cell signalling.<ref name="The Developing Human">Moore, K.L., Persaud, T.V.N. & Torchia, M.G. (2015). The developing human: clinically oriented embryology (10th ed.). Philadelphia: Saunders.</ref> | The Notch signalling pathway is critical for cell differentiation, proliferation, and apoptosis. It is involved in embryonic organ development through the regulation of cell-cell signalling; specifically lateral inhibition, formation of boundaries, and cell lineage assignation.<ref name="The Developing Human">Moore, K.L., Persaud, T.V.N. & Torchia, M.G. (2015). The developing human: clinically oriented embryology (10th ed.). Philadelphia: Saunders.</ref><ref name=PMID10075488><pubmed>10075488</pubmed></ref> | ||
===History=== | ===History=== | ||
===Overview of Molecular Mechanisms=== | ===Overview of Molecular Mechanisms=== | ||
Four NOTCH proteins are involved in the pathway. NOTCH1 to NOTCH4 are single transmembrane receptors and can interact with a variety of ligands, including NOTCH ligands (e.g. Delta | Four NOTCH proteins are involved in the canonical pathway. NOTCH1 to NOTCH4 are single transmembrane receptors and can interact with a variety of ligands, including NOTCH ligands (e.g. Delta ligands) and Serrate ligands (e.g. Jagged 1 [JAG1] and Jagged 2 [JAG2]). The binding between the Notch receptor and the ligand on adjacent cell induces the release of the Notch intracellular domain (NICD) via a sequence of proteolytic reactions.<ref name="The Developing Human"/> Cell-cell interaction is therefore critical in the process of triggering Notch signalling. The NICD enters the nucleus and interacts with the Suppressor of Hairless DNA-binding protein (Su(H)) to promote transcription of Notch target genes.<ref name=PMID10075488/> | ||
===Roles in development=== | ===Roles in development=== | ||
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===Abnormalities in Notch signalling=== | ===Abnormalities in Notch signalling=== | ||
====Alagille syndrome==== | ====Alagille syndrome==== | ||
Alagille syndrome (AGS) is an autosomal dominant, multisystem disorder that mainly affects the liver, heart, and kidney. In 94% of clinically diagnosed cases, a mutation in the gene encoding the Notch ligand JAG1 has been identified as a contributing factor. In combination with this, a mutation in the NOTCH2 gene has also been implicated in the diagnosis of AGS.<ref><pubmed>16773578</pubmed></ref> | |||
===Recent and Current Research=== | ===Recent and Current Research=== |
Revision as of 14:56, 2 September 2016
2016 Student Projects | ||||
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Signalling: 1 Wnt | 2 Notch | 3 FGF Receptor | 4 Hedgehog | 5 T-box | 6 TGF-Beta | ||||
2016 Group Project Topic - Signaling in Development
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Notch signalling pathway
Introduction
The Notch signalling pathway is critical for cell differentiation, proliferation, and apoptosis. It is involved in embryonic organ development through the regulation of cell-cell signalling; specifically lateral inhibition, formation of boundaries, and cell lineage assignation.[1][2]
History
Overview of Molecular Mechanisms
Four NOTCH proteins are involved in the canonical pathway. NOTCH1 to NOTCH4 are single transmembrane receptors and can interact with a variety of ligands, including NOTCH ligands (e.g. Delta ligands) and Serrate ligands (e.g. Jagged 1 [JAG1] and Jagged 2 [JAG2]). The binding between the Notch receptor and the ligand on adjacent cell induces the release of the Notch intracellular domain (NICD) via a sequence of proteolytic reactions.[1] Cell-cell interaction is therefore critical in the process of triggering Notch signalling. The NICD enters the nucleus and interacts with the Suppressor of Hairless DNA-binding protein (Su(H)) to promote transcription of Notch target genes.[2]
Roles in development
Cardiovascular
Central Nervous System
Other Systems
Animal models
Abnormalities in Notch signalling
Alagille syndrome
Alagille syndrome (AGS) is an autosomal dominant, multisystem disorder that mainly affects the liver, heart, and kidney. In 94% of clinically diagnosed cases, a mutation in the gene encoding the Notch ligand JAG1 has been identified as a contributing factor. In combination with this, a mutation in the NOTCH2 gene has also been implicated in the diagnosis of AGS.[3]
Recent and Current Research