From Wikipedia, the free encyclopedia
(Redirected from BAI3)
ADGRB3
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
Aliases ADGRB3, BAI3, adhesion G protein-coupled receptor B3
External IDs OMIM: 602684; MGI: 2441837; HomoloGene: 1289; GeneCards: ADGRB3; OMA: ADGRB3 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001704

NM_175642

RefSeq (protein)

NP_001695

NP_783573

Location (UCSC) Chr 6: 68.64 – 69.39 Mb Chr 1: 25.11 – 25.87 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Brain-specific angiogenesis inhibitor 3 is a protein that in humans is encoded by the BAI3 gene. [5] [6]

BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis. [6] The BAI3 receptor has also been found to regulate dendrite morphogenesis, arborization growth and branching in cultured neurons. [7]

The adhesion GPCR BaI3 is an orphan receptor that has a long N-terminus consisting of one cub domain, five BaI Thrombospondin type 1 repeats, and one hormone binding domain. [8] BaI3 is expressed in neural tissues of the central nervous system. BaI3 has been shown to have a high affinity for C1q proteins. C1q added to hippocampal neurons expressing BaI3 resulted in a decrease in the number of synapses.

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000135298Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000033569Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Shiratsuchi T, Nishimori H, Ichise H, Nakamura Y, Tokino T (Apr 1998). "Cloning and characterization of BAI2 and BAI3, novel genes homologous to brain-specific angiogenesis inhibitor 1 (BAI1)". Cytogenetics and Cell Genetics. 79 (1–2): 103–108. doi: 10.1159/000134693. PMID  9533023.
  6. ^ a b "Entrez Gene: BAI3 brain-specific angiogenesis inhibitor 3".
  7. ^ Lanoue, V; Usardi, A; Sigoillot, S M; Talleur, M; Iyer, K; Mariani, J; Isope, P; Vodjdani, G; Heintz, N; Selimi, F (2013). "The adhesion-GPCR BAI3, a gene linked to psychiatric disorders, regulates dendrite morphogenesis in neurons". Molecular Psychiatry. 18 (8): 943–950. doi: 10.1038/mp.2013.46. PMC  3730300. PMID  23628982.
  8. ^ Bolliger MF, Martinelli DC, Südhof TC (February 2011). "The cell-adhesion G protein-coupled receptor BAI3 is a high-affinity receptor for C1q-like proteins". Proceedings of the National Academy of Sciences of the United States of America. 108 (6): 2534–2539. Bibcode: 2011PNAS..108.2534B. doi: 10.1073/pnas.1019577108. PMC  3038708. PMID  21262840.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


From Wikipedia, the free encyclopedia
(Redirected from BAI3)
ADGRB3
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
Aliases ADGRB3, BAI3, adhesion G protein-coupled receptor B3
External IDs OMIM: 602684; MGI: 2441837; HomoloGene: 1289; GeneCards: ADGRB3; OMA: ADGRB3 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001704

NM_175642

RefSeq (protein)

NP_001695

NP_783573

Location (UCSC) Chr 6: 68.64 – 69.39 Mb Chr 1: 25.11 – 25.87 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Brain-specific angiogenesis inhibitor 3 is a protein that in humans is encoded by the BAI3 gene. [5] [6]

BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis. [6] The BAI3 receptor has also been found to regulate dendrite morphogenesis, arborization growth and branching in cultured neurons. [7]

The adhesion GPCR BaI3 is an orphan receptor that has a long N-terminus consisting of one cub domain, five BaI Thrombospondin type 1 repeats, and one hormone binding domain. [8] BaI3 is expressed in neural tissues of the central nervous system. BaI3 has been shown to have a high affinity for C1q proteins. C1q added to hippocampal neurons expressing BaI3 resulted in a decrease in the number of synapses.

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000135298Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000033569Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Shiratsuchi T, Nishimori H, Ichise H, Nakamura Y, Tokino T (Apr 1998). "Cloning and characterization of BAI2 and BAI3, novel genes homologous to brain-specific angiogenesis inhibitor 1 (BAI1)". Cytogenetics and Cell Genetics. 79 (1–2): 103–108. doi: 10.1159/000134693. PMID  9533023.
  6. ^ a b "Entrez Gene: BAI3 brain-specific angiogenesis inhibitor 3".
  7. ^ Lanoue, V; Usardi, A; Sigoillot, S M; Talleur, M; Iyer, K; Mariani, J; Isope, P; Vodjdani, G; Heintz, N; Selimi, F (2013). "The adhesion-GPCR BAI3, a gene linked to psychiatric disorders, regulates dendrite morphogenesis in neurons". Molecular Psychiatry. 18 (8): 943–950. doi: 10.1038/mp.2013.46. PMC  3730300. PMID  23628982.
  8. ^ Bolliger MF, Martinelli DC, Südhof TC (February 2011). "The cell-adhesion G protein-coupled receptor BAI3 is a high-affinity receptor for C1q-like proteins". Proceedings of the National Academy of Sciences of the United States of America. 108 (6): 2534–2539. Bibcode: 2011PNAS..108.2534B. doi: 10.1073/pnas.1019577108. PMC  3038708. PMID  21262840.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.



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