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Deficiency of BLNK hampers PLC-gamma2 phosphorylation and Ca2+ influx induced by the pre-B-cell receptor in human pre-B cells.
Immunology. 2004 Aug; 112(4):575-82.I

Abstract

B-cell linker protein (BLNK) is a component of the B-cell receptor (BCR) as well as of the pre-BCR signalling pathway, and BLNK(-/-) mice have a block in B lymphopoiesis at the pro-B/pre-B cell stage. A recent report described the complete loss or drastic reduction of BLNK expression in approximately 50% of human childhood pre-B acute lymphoblastic leukaemias (ALL), therefore we investigated BLNK expression in human pre-B ALL cell lines. One of the four cell lines tested, HPB-NULL cells, was found to lack BLNK expression, and we used these human pre-B ALL cell lines that express and do not express BLNK to investigate the intracellular signalling events following pre-BCR cross-linking. When pre-BCR was cross-linked with anti-micro heavy-chain antibodies, significant phosphorylation of intracellular molecules, including Syk, Shc, ERK MAP kinase, and AKT, and an activation of Ras were observed without regard to deficiency of BLNK expression, suggesting that BLNK is not required for pre-BCR-mediated activation of MAP kinase and phosphatidyl-inositol 3 (PI3) kinase signalling. By contrast, phospholipase C-gamma2 (PLC-gamma2) phosphorylation and an increase in intracellular Ca(2+) level mediated by pre-BCR cross-linking were observed only in the BLNK-expressing cells, indicating that BLNK is essential for PLC-gamma2-induced Ca(2+) influx. Human pre-B cell lines expressing and not expressing BLNK should provide an in vitro model for investigation of the role of BLNK in the pre-BCR-mediated signalling mechanism.

Authors+Show Affiliations

Department of Developmental Biology, National Research Institute for Child Health and Development, 3-35-31 Taishido, Setagaya-ku, Tokyo 154-8567, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15270728

Citation

Taguchi, Tomoko, et al. "Deficiency of BLNK Hampers PLC-gamma2 Phosphorylation and Ca2+ Influx Induced By the pre-B-cell Receptor in Human pre-B Cells." Immunology, vol. 112, no. 4, 2004, pp. 575-82.
Taguchi T, Kiyokawa N, Takenouch H, et al. Deficiency of BLNK hampers PLC-gamma2 phosphorylation and Ca2+ influx induced by the pre-B-cell receptor in human pre-B cells. Immunology. 2004;112(4):575-82.
Taguchi, T., Kiyokawa, N., Takenouch, H., Matsui, J., Tang, W. R., Nakajima, H., Suzuki, K., Shiozawa, Y., Saito, M., Katagiri, Y. U., Takahashi, T., Karasuyama, H., Matsuo, Y., Okita, H., & Fujimoto, J. (2004). Deficiency of BLNK hampers PLC-gamma2 phosphorylation and Ca2+ influx induced by the pre-B-cell receptor in human pre-B cells. Immunology, 112(4), 575-82.
Taguchi T, et al. Deficiency of BLNK Hampers PLC-gamma2 Phosphorylation and Ca2+ Influx Induced By the pre-B-cell Receptor in Human pre-B Cells. Immunology. 2004;112(4):575-82. PubMed PMID: 15270728.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Deficiency of BLNK hampers PLC-gamma2 phosphorylation and Ca2+ influx induced by the pre-B-cell receptor in human pre-B cells. AU - Taguchi,Tomoko, AU - Kiyokawa,Nobutaka, AU - Takenouch,Hisami, AU - Matsui,Jun, AU - Tang,Wei-Ran, AU - Nakajima,Hideki, AU - Suzuki,Kyoko, AU - Shiozawa,Yusuke, AU - Saito,Masahiro, AU - Katagiri,Yohko U, AU - Takahashi,Takao, AU - Karasuyama,Hajime, AU - Matsuo,Yoshinobu, AU - Okita,Hajime, AU - Fujimoto,Junichiro, PY - 2004/7/24/pubmed PY - 2004/9/21/medline PY - 2004/7/24/entrez SP - 575 EP - 82 JF - Immunology JO - Immunology VL - 112 IS - 4 N2 - B-cell linker protein (BLNK) is a component of the B-cell receptor (BCR) as well as of the pre-BCR signalling pathway, and BLNK(-/-) mice have a block in B lymphopoiesis at the pro-B/pre-B cell stage. A recent report described the complete loss or drastic reduction of BLNK expression in approximately 50% of human childhood pre-B acute lymphoblastic leukaemias (ALL), therefore we investigated BLNK expression in human pre-B ALL cell lines. One of the four cell lines tested, HPB-NULL cells, was found to lack BLNK expression, and we used these human pre-B ALL cell lines that express and do not express BLNK to investigate the intracellular signalling events following pre-BCR cross-linking. When pre-BCR was cross-linked with anti-micro heavy-chain antibodies, significant phosphorylation of intracellular molecules, including Syk, Shc, ERK MAP kinase, and AKT, and an activation of Ras were observed without regard to deficiency of BLNK expression, suggesting that BLNK is not required for pre-BCR-mediated activation of MAP kinase and phosphatidyl-inositol 3 (PI3) kinase signalling. By contrast, phospholipase C-gamma2 (PLC-gamma2) phosphorylation and an increase in intracellular Ca(2+) level mediated by pre-BCR cross-linking were observed only in the BLNK-expressing cells, indicating that BLNK is essential for PLC-gamma2-induced Ca(2+) influx. Human pre-B cell lines expressing and not expressing BLNK should provide an in vitro model for investigation of the role of BLNK in the pre-BCR-mediated signalling mechanism. SN - 0019-2805 UR - https://www.unboundmedicine.com/medline/citation/15270728/Deficiency_of_BLNK_hampers_PLC_gamma2_phosphorylation_and_Ca2+_influx_induced_by_the_pre_B_cell_receptor_in_human_pre_B_cells_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=15270728.ui DB - PRIME DP - Unbound Medicine ER -