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Purinergic receptor P2Y, G-protein coupled, 8

P2RY8, p2y8
The protein encoded by this gene belongs to the family of G-protein coupled receptors, that are preferentially activated by adenosine and uridine nucleotides. This gene is moderately expressed in undifferentiated HL60 cells, and is located on both chromosomes X and Y. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, JAK2, iMpact, p16, Pax5
Papers on P2RY8
CRLF2 overexpression identifies an unfavourable subgroup of adult B-cell precursor acute lymphoblastic leukemia lacking recurrent genetic abnormalities.
Foà et al., Roma, Italy. In Leuk Res, Jan 2016
Incidence and clinical impact of the P2RY8/CRLF2 transcript was also assessed.
The G protein-coupled receptor P2RY8 and follicular dendritic cells promote germinal center confinement of B cells, whereas S1PR3 can contribute to their dissemination.
Cyster et al., San Francisco, United States. In J Exp Med, Jan 2016
The orphan Gα13-coupled receptor P2RY8 is mutated in human germinal center (GC)-derived lymphomas and was recently found to promote B cell association with GCs in a mouse model.
The clinical impact of IKZF1 deletions in paediatric B-cell precursor acute lymphoblastic leukaemia is independent of minimal residual disease stratification in Nordic Society for Paediatric Haematology and Oncology treatment protocols used between 1992 and 2013.
Johansson et al., Lund, Sweden. In Br J Haematol, Sep 2015
(P2RY8-CRLF2) and ∆IKZF1 increased the risk of relapse (75% vs. 30% for cases with only ∆IKZF1; P = 0·045), indicating that BCP-other ALL with both P2RY8-CRLF2 and ∆IKZF1 constitutes a particularly high-risk group.
Loss of signalling via Gα13 in germinal centre B-cell-derived lymphoma.
Cyster et al., San Francisco, United States. In Nature, 2015
The incomplete phenocopy of Gα13- and S1PR2 deficiency led us to discover that P2RY8, an orphan receptor that is mutated in GCB-DLBCL and another germinal centre B-cell-derived malignancy, Burkitt's lymphoma, also represses germinal centre B-cell growth and promotes confinement via Gα13.
Lymphocyte gene expression signatures from patients and mouse models of hereditary hemochromatosis reveal a function of HFE as a negative regulator of CD8+ T-lymphocyte activation and differentiation in vivo.
Porto et al., Porto, Portugal. In Plos One, 2014
HH patients with low CD8+ T-lymphocyte numbers show a differential expression of genes related to lymphocyte differentiation and maturation namely CCR7, LEF1, ACTN1, NAA50, P2RY8 and FOSL2, whose expression correlates with the relative proportions of naïve, central and effector memory subsets.
Gene alterations involving the CRLF2-JAK pathway and recurrent gene deletions in Down syndrome-associated acute lymphoblastic leukemia in Japan.
Ito et al., Hirosaki, Japan. In Genes Chromosomes Cancer, 2014
We confirmed a high incidence of P2RY8-CRLF2 (29%) and JAK2 mutations (16%), though the frequency of P2RY8-CRLF2 was slightly lower than that in Western countries (∼50%).
An overall characterization of pediatric acute lymphoblastic leukemia with CRLF2 overexpression.
Japan Association of Childhood Leukemia Study et al., Kyoto, Japan. In Genes Chromosomes Cancer, 2014
CRLF2 OE was detected in 30 (18%) of 167 patients, the P2RY8-CRLF2 fusion was identified in only 3 (1.8%) of 167 patients, all of which demonstrated CRLF2 OE.
Frequent cases of RAS-mutated Down syndrome acute lymphoblastic leukaemia lack JAK2 mutations.
Antonarakis et al., Genève, Switzerland. In Nat Commun, 2013
Here, using full-exome or cancer genes-targeted sequencing of 42 ALL samples from 39 DS patients, we uncover driver mutations in RAS, (KRAS and NRAS) recurring to a similar extent (15/42) as JAK2 (12/42) mutations or P2RY8-CRLF2 fusions (14/42).
An mRNA atlas of G protein-coupled receptor expression during primary human monocyte/macrophage differentiation and lipopolysaccharide-mediated activation identifies targetable candidate regulators of inflammation.
Sweet et al., Brisbane, Australia. In Immunobiology, 2013
P2RY8, GPR92, EMR3) have not been widely investigated in macrophage biology and inflammation.
IKZF1 deletion is associated with a poor outcome in pediatric B-cell precursor acute lymphoblastic leukemia in Japan.
Japan Association of Childhood Leukemia Study (JACLS) et al., Kyoto, Japan. In Cancer Med, 2013
Herein, we conducted genetic analyses of IKZF1 deletion, point mutation of JAK2 exon 16, 17, and 21, CRLF2 expression, the presence of P2RY8-CRLF2 fusion and F232C mutation in CRLF2 in 202 pediatric BCP-ALL patients newly diagnosed and registered in Japan Childhood Leukemia Study ALL02 protocol to find out if alterations in these genes are determinants of poor outcome.
IKZF1 deletion is an independent predictor of outcome in pediatric acute lymphoblastic leukemia treated according to the ALL-BFM 2000 protocol.
Cario et al., Kiel, Germany. In Haematologica, 2013
Although IKZF1 deletions were significantly associated with the P2RY8-CRLF2 rearrangement, their prognostic value was found to be independent from this association.
Small sizes and indolent evolutionary dynamics challenge the potential role of P2RY8-CRLF2-harboring clones as main relapse-driving force in childhood ALL.
Panzer-Grümayer et al., Vienna, Austria. In Blood, 2013
The P2RY8-CRLF2 fusion defines a particular relapse-prone subset of childhood acute lymphoblastic leukemia (ALL) in Italian Association of Pediatric Hematology and Oncology Berlin-Frankfurt-Münster (AIEOP-BFM) 2000 protocols.
IGH@ translocations, CRLF2 deregulation, and microdeletions in adolescents and adults with acute lymphoblastic leukemia.
Harrison et al., Newcastle upon Tyne, United Kingdom. In J Clin Oncol, 2012
RESULTS: Twenty patients (5%) had CRLF2-d (P2RY8-CRLF2, n = 7; IGH@-CRLF2, n = 13), and 36 patients (8%) harbored an IGH@-t with a different partner gene.
Presence of the P2RY8-CRLF2 rearrangement is associated with a poor prognosis in non-high-risk precursor B-cell acute lymphoblastic leukemia in children treated according to the ALL-BFM 2000 protocol.
Stanulla et al., Kiel, Germany. In Blood, 2010
Study reports an extremely high incidence of relapse (71% +/- 19%) in non-high-risk precursor B-cell acute lymphoblastic leukemia patients with P2RY8-CRLF2 rearrangement.
Rearrangement of CRLF2 in B-progenitor- and Down syndrome-associated acute lymphoblastic leukemia.
Rabin et al., In Nat Genet, 2009
Here we report a recurring interstitial deletion of the pseudoautosomal region 1 of chromosomes X and Y in B-progenitor ALL that juxtaposes the first, noncoding exon of P2RY8 with the coding region of CRLF2.
Upregulation of the SOX5 by promoter swapping with the P2RY8 gene in primary splenic follicular lymphoma.
Rocchi et al., In Leukemia, 2007
SOX5 is upregulated by promoter swapping with the P2RY8 gene in primary splenic follicular lymphoma
Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening.
Mano et al., Tochigi, Japan. In Leuk Lymphoma, 2007
P2RY8 is expressed in leukemic cells and has an unexpected role in the pathogenesis of acute leukemia
Molecular pharmacology of P2Y-receptors.
Wetter et al., Bonn, Germany. In Naunyn Schmiedebergs Arch Pharmacol, 2000
The P2Y3-, p2y8- and tp2y-receptors may be species orthologues.
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