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Titolo:
CD19 amplification of B lymphocyte Ca2+ responses - A role for Lyn sequestration in extinguishing negative regulation
Autore:
Fujimoto, M; Poe, JC; Hasegawa, M; Tedder, TF;
Indirizzi:
Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 Med Ctr, Dept Immunol, Durham, NC 27710 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 48, volume: 276, anno: 2001,
pagine: 44820 - 44827
SICI:
0021-9258(20011130)276:48<44820:CAOBLC>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL ANTIGEN RECEPTOR; PROTEIN-TYROSINE KINASE; SIGNAL-TRANSDUCTION MOLECULE; CYTOPLASMIC DOMAIN; PHOSPHATIDYLINOSITOL 3-KINASE; MEDIATED ACTIVATION; CD22-DEFICIENT MICE; PHOSPHATASE 1C; CD22; COMPLEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
66
Recensione:
Indirizzi per estratti:
Indirizzo: Tedder, TF Duke Univ, Med Ctr, Dept Immunol, Box 3010, Durham, NC 27710 USA Duke Univ Box 3010 Durham NC USA 27710 10, Durham, NC 27710 USA
Citazione:
M. Fujimoto et al., "CD19 amplification of B lymphocyte Ca2+ responses - A role for Lyn sequestration in extinguishing negative regulation", J BIOL CHEM, 276(48), 2001, pp. 44820-44827

Abstract

B lymphocyte antigen receptor (BCR) signals are regulated by CD19, with BCR-induced intracellular calcium ([Ca2+](i)) responses enhanced by CD19 co-ligation. In this study, CD19 engagement using a dimeric anti-CD19 antibody induced [Ca2+](i) mobilization and significantly enhanced BCR-induced [Ca2+](i) responses without a requirement for CD19/BCR co-ligation. Although simultaneous CD19 and BCR engagement significantly enhanced CD19/Lyn complex formation and [Ca2+](i) responses, downstream tyrosine phosphorylation of CD22 and multiple other cellular proteins was inhibited, as teas SHP1 recruitment to phosphorylated CD22. CD19 overexpression also enhanced BCR-induced [Ca2+](i) responses, but down-regulated tyrosine phosphorylation of CD22 and multiple other cellular proteins following BCR ligation. Because CD19 andLyn expression are genetically titrated in B cells, CD19 engagement may augment BCR-induced [Ca2+](i) responses by sequestering the available pool offunctional Lyn away from downstream negative regulatory proteins such as CD22. Consistent with this, simultaneous CD19 engagement did not further enhance the BCR-induced [Ca2+](i) responses of Lyn- or CD22-deficient B cells. Thus, CD19 recruitment of Lyn may preferentially activate selective signaling pathways downstream of the CD19/Lyn complex to the exclusion of other downstream regulatory and effector pathways. Other receptors may also utilize a similar strategy to regulate kinase availability and downstream intermolecular signaling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 20:29:03