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Brain-specific angiogenesis inhibitor 1

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ADGRB1
Identifiers
AliasesADGRB1, BAI1, GDAIF, adhesion G protein-coupled receptor B1
External IDsOMIM: 602682; MGI: 1933736; HomoloGene: 1287; GeneCards: ADGRB1; OMA:ADGRB1 - orthologs
Orthologs
SpeciesHumanMouse
Entrez

575

107831

Ensembl

ENSG00000181790

ENSMUSG00000034730

UniProt

O14514

Q3UHD1

RefSeq (mRNA)

NM_001702
NM_001391985
NM_001391986
NM_001391987
NM_001391988

NM_174991
NM_001359759

RefSeq (protein)

NP_001693

NP_778156
NP_001346688

Location (UCSC)Chr 8: 142.45 – 142.55 MbChr 15: 74.39 – 74.46 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Brain-specific angiogenesis inhibitor 1 is a protein that in humans is encoded by the BAI1 gene.[5][6] It is a member of the adhesion-GPCR family of receptors.[7]

Function

Angiogenesis is controlled by a local balance between stimulators and inhibitors of new vessel growth and is suppressed under normal physiologic conditions. Angiogenesis has been shown to be essential for growth and metastasis of solid tumors. In order to obtain blood supply for their growth, tumor cells are potently angiogenic and attract new vessels as results of increased secretion of inducers and decreased production of endogenous negative regulators. BAI1 contains at least one 'functional' p53-binding site within an intron, and its expression has been shown to be induced by wildtype p53. There are two other brain-specific angiogenesis inhibitor genes, designated BAI2 and BAI3 which along with BAI1 have similar tissue specificities and structures, however only BAI1 is transcriptionally regulated by p53. BAI1 is postulated to be a member of the secretin receptor family, an inhibitor of angiogenesis and a growth suppressor of glioblastomas.[6]

Interactions

Brain-specific angiogenesis inhibitor 1 has been shown to interact with BAIAP3[8] and MAGI1.[9]

Model organisms

Model organisms have been used in the study of BAI1 function. A conditional knockout mouse line called Bai1tm2a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute.[10] Male and female animals underwent a standardized phenotypic screen[11] to determine the effects of deletion.[12][13][14][15] Additional screens performed: - In-depth immunological phenotyping[16] - in-depth bone and cartilage phenotyping[17]

Bai1 knockout mouse phenotype
Characteristic Phenotype
All data available at.[11][16][17]
Peripheral blood leukocytes 6 Weeks Normal
Haematology 6 Weeks Normal
Insulin Normal
Homozygous viability at P14 Normal
Homozygous Fertility Normal
General Observations Abnormal
Body weight Normal
Neurological assessment Normal
Grip strength Normal
Dysmorphology Normal
Indirect calorimetry Normal
Glucose tolerance test Normal
Auditory brainstem response Abnormal
DEXA Normal
Radiography Normal
Eye morphology Normal
Clinical chemistry Normal
Haematology 16 Weeks Abnormal
Peripheral blood leukocytes 16 Weeks Abnormal
Heart weight Normal
Salmonella infection Normal
Spleen Immunophenotyping Normal
Mesenteric Lymph Node Immunophenotyping Normal
Epidermal Immune Composition Normal



References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000181790 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000034730 – Ensembl, 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): 103–8. doi:10.1159/000134693. PMID 9533023.
  6. ^ a b "Entrez Gene: BAI1 brain-specific angiogenesis inhibitor 1".
  7. ^ Stacey M, Yona S (2011). AdhesionGPCRs: Structure to Function (Advances in Experimental Medicine and Biology). Berlin: Springer. ISBN 978-1-4419-7912-4.
  8. ^ Shiratsuchi T, Oda K, Nishimori H, Suzuki M, Takahashi E, Tokino T, Nakamura Y (Oct 1998). "Cloning and characterization of BAP3 (BAI-associated protein 3), a C2 domain-containing protein that interacts with BAI1". Biochemical and Biophysical Research Communications. 251 (1): 158–65. doi:10.1006/bbrc.1998.9408. PMID 9790924.
  9. ^ Shiratsuchi T, Futamura M, Oda K, Nishimori H, Nakamura Y, Tokino T (Jun 1998). "Cloning and characterization of BAI-associated protein 1: a PDZ domain-containing protein that interacts with BAI1". Biochemical and Biophysical Research Communications. 247 (3): 597–604. doi:10.1006/bbrc.1998.8603. PMID 9647739.
  10. ^ Gerdin AK (2010). "The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x. S2CID 85911512.
  11. ^ a b "International Mouse Phenotyping Consortium".
  12. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  13. ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  14. ^ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. S2CID 18872015.
  15. ^ White JK, Gerdin AK, Karp NA, Ryder E, Buljan M, Bussell JN, Salisbury J, Clare S, Ingham NJ, Podrini C, Houghton R, Estabel J, Bottomley JR, Melvin DG, Sunter D, Adams NC, Sanger Institute Mouse Genetics Project, Tannahill D, Logan DW, Macarthur DG, Flint J, Mahajan VB, Tsang SH, Smyth I, Watt FM, Skarnes WC, Dougan G, Adams DJ, Ramirez-Solis R, Bradley A, Steel KP (2013). "Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes". Cell. 154 (2): 452–64. doi:10.1016/j.cell.2013.06.022. PMC 3717207. PMID 23870131.
  16. ^ a b "Infection and Immunity Immunophenotyping (3i) Consortium".
  17. ^ a b "OBCD Consortium".

Further reading

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

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