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LAB/NTAL/Lat2: a force to be reckoned with in all leukocytes?

  1. Author:
    Orr, S. J.
    McVicar, D. W.

  2. Author Address

    [Orr, Selinda J.; McVicar, Daniel W.] NCI, Canc & Inflammat Program, Frederick, MD 21702 USA.;McVicar, DW, NCI, Canc & Inflammat Program, Bldg 560,Rm 31-46, Frederick, MD 21702 USA.;mcvicard@mail.nih.gov
    1. Year: 2011
    2. Date: Jan
  2. Journal: Journal of Leukocyte Biology
    1. 89
    2. 1
    3. Pages: 11-19
  4. Type of Article: Article
  5. ISSN: 0741-5400
  1. Abstract:

    LAB/NTAL/Lat2 is a transmembrane adaptor protein closely related to LAT. It is expressed in various myeloid and lymphoid cells, many of which also express LAT. Phosphorylation of LAB occurs following engagement of various ITAM- and non-ITAM-linked receptors and can play positive and negative roles following receptor engagement. LAT binds PLC gamma directly, resulting in efficient Ca2+ flux and degranulation. However, LAB does not contain a PLC gamma-binding motif and only binds PLC gamma indirectly, possibly via Grb2, thereby resulting in suboptimal signaling. As LAT can signal more efficiently than LAB, competition between the 2 for space/substrates in the lipid rafts can attenuate signaling. This competition model requires coexpression of LAT; however, LAB is repressive, even in cells lacking substantial LAT expression such as macrophages and mature B cells. The reported interaction between LAB and the ubiquitin E3-ligase c-Cbl suggests 1 possible mechanism for LAT-independent inhibition by LAB, but such a model requires further investigation. Given the wide-reaching expression pattern of LAB, LAB has the ability to modulate signaling in virtually every type of leukocyte. Regardless of its ultimate mode of action, the potent regulatory capability of LAB proves this protein to be a complex adaptor that warrants continued, substantial scrutiny by biochemists and immunologists alike. J. Leukoc. Biol. 89: 11-19; 2011.

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External Sources

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  2. DOI: 10.1189/jlb.0410221
  3. View record in Web of Science®
  4. WOS: 000285866400003

Library Notes

  1. Fiscal Year: FY2010-2011
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