DUSP5

From Wikipedia, the free encyclopedia
Jump to: navigation, search
DUSP5
Protein DUSP5 PDB 2g6z.png
Available structures
PDB Human UniProt search: PDBe RCSB
Identifiers
Aliases DUSP5, DUSP, HVH3, dual specificity phosphatase 5
External IDs MGI: 2685183 HomoloGene: 3256 GeneCards: DUSP5
RNA expression pattern
PBB GE DUSP5 209457 at fs.png
More reference expression data
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_004419

NM_001085390

RefSeq (protein)

NP_004410

n/a

Location (UCSC) Chr 10: 110.5 – 110.51 Mb Chr 19: 53.53 – 53.54 Mb
PubMed search [1] [2]
Wikidata
View/Edit Human View/Edit Mouse

Dual specificity protein phosphatase 5 is an enzyme that in humans is encoded by the DUSP5 gene.[3][4]

Function[edit]

The protein encoded by this gene is a member of the dual specificity protein phosphatase subfamily. These phosphatases inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. They negatively regulate members of the mitogen-activated protein (MAP) kinase superfamily (MAPK/ERK, SAPK/JNK, p38), which are associated with cellular proliferation and differentiation. Different members of the family of dual specificity phosphatases show distinct substrate specificities for various MAP kinases, different tissue distribution and subcellular localization, and different modes of inducibility of their expression by extracellular stimuli. This gene product inactivates ERK1/2, is expressed in a variety of tissues with the highest levels in pancreas and brain, and is localized in the nucleus.[4]

Model organisms[edit]

Model organisms have been used in the study of DUSP5 function. A conditional knockout mouse line called Dusp5tm1a(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute.[5] Male and female animals underwent a standardized phenotypic screen[6] to determine the effects of deletion.[7][8][9][10] Additional screens performed: - In-depth immunological phenotyping[11]

References[edit]

  1. ^ "Human PubMed Reference:". 
  2. ^ "Mouse PubMed Reference:". 
  3. ^ Martell KJ, Kwak S, Hakes DJ, Dixon JE, Trent JM (Jul 1994). "Chromosomal localization of four human VH1-like protein-tyrosine phosphatases". Genomics. 22 (2): 462–4. doi:10.1006/geno.1994.1411. PMID 7806236. 
  4. ^ a b "Entrez Gene: DUSP5 dual specificity phosphatase 5". 
  5. ^ 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. 
  6. ^ a b "International Mouse Phenotyping Consortium". 
  7. ^ 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 3572410Freely accessible. PMID 21677750. 
  8. ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718. 
  9. ^ 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. 
  10. ^ 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, 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 (Jul 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 3717207Freely accessible. PMID 23870131. 
  11. ^ a b "Infection and Immunity Immunophenotyping (3i) Consortium". 

Further reading[edit]