Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Rel/NF-kappaB can trigger the Notch signaling pathway by inducing the expression of Jagged1, a ligand for Notch receptors.
A non-transmembrane form of Jagged-1 regulates the formation of matrix-dependent chord-like structures.
Physical interaction of Delta1, Jagged1, and Jagged2 with Notch1 and Notch3 receptors.
The notch ligand jagged-1 represents a novel growth factor of human hematopoietic stem cells.
Soluble Jagged 1 represses the function of its transmembrane form to induce the formation of the Src-dependent chord-like phenotype.
Members of the Jagged/Notch gene families are expressed in injured arteries and regulate cell phenotype via alterations in cell matrix and cell-cell interaction.
Jagged-1 mediated activation of notch signaling induces complete maturation of human keratinocytes through NF-kappaB and PPARgamma.
A conserved face of the Jagged/Serrate DSL domain is involved in Notch trans-activation and cis-inhibition.
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Conserved DSL face of Jagged-1 mediates both cis- and trans-interactions with Notch.
"The structure reveals a highly conserved face of the DSL domain, and we show, by functional analysis of Drosophila melanogster ligand mutants, that this surface is required for both cis- and trans-regulatory interactions with Notch."
Notch signaling is required for maintaining stem-cell features of neuroprogenitor cells derived from human embryonic stem cells.
Jagged1 (JAG1) mutations in patients with tetralogy of Fallot or pulmonic stenosis.
NOTCH1 missense alleles associated with left ventricular outflow tract defects exhibit impaired receptor processing and defective EMT.
Flexibility of the PDZ-binding motif in the micelle-bound form of Jagged-1 cytoplasmic tail.
The CD46-Jagged1 interaction is critical for human TH1 immunity.
A tail of two sites: a bipartite mechanism for recognition of notch ligands by mind bomb E3 ligases.
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MIB1 recognises two epitopes in the JAG1 cytoplasmic tail.
"Mib1 contains two independent substrate recognition domains that engage two distinct epitopes from the cytoplasmic tail of the ligand Jagged1, one in the intracellular membrane proximal region and the other near the C terminus."
Inactivation of the serine protease HTRA1 inhibits tumor growth by deregulating angiogenesis.
Dominant mutations of the Notch ligand Jagged1 cause peripheral neuropathy.
A physical wiring diagram for the human immune system.
Quantitative fragmentomics allow affinity mapping of interactomes.
Expression patterns of Jagged, Delta1, Notch1, Notch2, and Notch3 genes identify ligand-receptor pairs that may function in neural development.
An antisense oligonucleotide to the notch ligand jagged enhances fibroblast growth factor-induced angiogenesis in vitro.
Mutations in the human Jagged1 gene are responsible for Alagille syndrome.
Alagille syndrome is caused by mutations in human Jagged1, which encodes a ligand for Notch1.
Identification and cloning of the human homolog (JAG1) of the rat Jagged1 gene from the Alagille syndrome critical region at 20p12.
ADAM10/17 cleaves ligand-bound NOTCH1 PEST domain mutants to produce NEXT1 PEST domain mutants
NOTCH1 HD+PEST domain mutants are cleaved by ADAM10/17 irrespective of ligand binding
NOTCH1 t(7;9)(NOTCH1:M1580_K2555) does not bind JAG1
NOTCH1 HD domain mutants bind JAG1
NOTCH1 HD domain mutants are cleaved to produce NEXT1 irrespective of ligand binding
Ubiquitination of DLL/JAG ligands upon binding to NOTCH1 HD domain mutants
NOTCH1 PEST domain mutants bind JAG1
Ubiquitination of DLL/JAG ligands upon binding to NOTCH1 PEST domain mutants
NOTCH1 HD+PEST domain mutants bind JAG1
Ubiquitination of DLL/JAG ligands upon binding to NOTCH1 HD+PEST domain mutants
JAG1 gene expression is inhibited by RUNX3
NOTCH3-ligand complex is cleaved to produce NEXT3
Falcon deep research report on human JAG1
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JAG1 cis-inhibition strength is receptor-dependent.
"However, the strength of JAG1-mediated cis-inhibition varies by receptor: JAG1 does not produce robust Notch1 cis-inhibition because it fails to form the homodimers required for full cis-blockade, unlike DLL4 or JAG2"
UniProtKB entry P78504 (JAG1_HUMAN)