The T11 glycoprotein is functionally linked to a calcium channel in precursor and mature T-lineage cells.

Alcover, Andrés; Weiss, Michael J.; Daley, John; Reinherz, Ellis L.

doi:10.1073/pnas.83.8.2614

Cited by 84 publications

(45 citation statements)

References 20 publications

(15 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CD2 expression under the conditions used. Retained CD2 expression is significant because some authors have suggested that T cell receptor/CD3 complex-mediated activation may be tied to the CD2 machinery (45).…”

Section: Resultsmentioning

confidence: 99%

Bacterial toxins affect early events of T lymphocyte activation.

Stewart¹,

Prpić²,

Johns³

et al. 1989

J. Clin. Invest.

View full text Add to dashboard Cite

The effects of pertussis toxin and cholera toxin on early events of T lymphocyte activation were examined in the T lymphocyte cell line, Jurkat. Pertussis toxin treatment of these T cells increased inositol phosphates production and led to increases in intracellular free calcium concentration. These effects were produced by the isolated B (binding) subunit of pertussis toxin, alone. Inositol phosphates production resulting from perturbation of the T cell antigen receptor-CD3 complex by MAb was not affected by pertussis toxin treatment but was markedly inhibited by cholera toxin. This effect of cholera toxin paralleled elevations in cAMP content. However, forskolin, in concentrations equipotent for cAMP production, was a weaker inhibitor of inositol phosphates production. Cholera toxin inhibition of inositol phosphates production did not result from inhibition of baseline incorporation of inositol into phosphoinositide substrates of phospholipase C. These studies underline the complexity of toxin effects on cellular systems and suggest that other approaches will be required to implicate guanine nucleotide-binding regulatory proteins in control of the early events of T lymphocyte activation. However, the data presented here provide a molecular basis for the clinical observations of lymphocytosis and the in vitro observations of lymphocyte mitogenesis after pertussis toxin stimulation.

show abstract

Section: Resultsmentioning

confidence: 99%

Bacterial toxins affect early events of T lymphocyte activation.

Stewart¹,

Prpić²,

Johns³

et al. 1989

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…T-cell activation by mitogens (41), antigens (42), or monoclonal antibodies against the T3/T-cell receptor protein complex (43) or the T11 glycoprotein (44) results in an increase in cytoplasmic free Ca2". This has led a number of groups to postulate the existence of at least a Ca2+ channel linked to the T11 structure and/or T3/T-cell receptor complex (40,44).…”

Section: Discussionmentioning

confidence: 99%

cDNA cloning and sequence of MAL, a hydrophobic protein associated with human T-cell differentiation.

Alonso¹,

Weissman²

1987

Proc. Natl. Acad. Sci. U.S.A.

148

137

View full text Add to dashboard Cite

We have isolated a human cDNA that is expressed in the intermediate and late stages of T-cell differentiation. The cDNA encodes a highly hydrophobic protein, termed MAL, that lacks a hydrophobic leader peptide sequence and contains four potential transmembrane domains separated by short hydrophilic segments. The predicted configuration of the MAL protein resembles the structure of integral proteins that form pores or channels in the plasma membrane and that are believed to act as transporters of water-soluble molecules and ions across the lipid bilayer. The presence of MAL mRNA in a panel of T-cell Total cytoplasmic RNA from tissue culture cells was prepared by the Nonidet P-40 lysis method (6). Membranebound RNA was prepared by mechanical disruption of cells in hypotonic buffer and differential centrifugation (7). When frozen tissues were used, total RNA was isolated by homogenization in 4 M guanidinium thiocyanate, followed by ultracentrifugation through a 5.7 M CsCl cushion (8). Poly-(A)' RNA was isolated by oligo(dT)-cellulose chromatography (9). High molecular weight genomic DNA was prepared essentially as described by Maniatis et al. (10).The first strand of cDNA was synthesized by oligo(dT) priming using poly(A)+ RNA from MOLT-4 cells and avian myeloblastosis virus reverse transcriptase (Life Sciences, St. Petersburg, FL) in the presence of actinomycin D at 100 ng/ml. This cDNA was mixed with a 10-fold mass excess of poly(A)+ RNA from CCRF HSB-2 cells, boiled for 60 sec, and incubated at 680C in 0.5 M phosphate buffer, pH 6.8/5 mM EDTA/0. 1% NaDodSO4 to a Rot (initial concentration of RNA x time) value of 1500 (11). Unhybridized cDNA was separated from the cDNA RNA hybrids by chromatography on a hydroxyapatite column using 0.12 M phosphate buffer, pH 6.8/0.1% NaDodSO4 at 60°C. This single-stranded cDNA fraction was then used to construct libraries in the EcoRI site of pBR322 (10) and bacteriophage XgtlO (12). The second strand was synthesized by using RNase H, Escherichia coli DNA polymerase, and T4 DNA ligase (13). cDNA molecules >800 base pairs long were cloned in the unique EcoRI site of XgtlO. Subtracted [32P]cDNA probes were generated using a similar protocol except that the cDNA was labeled to specific activities of up to 109 cpm/,ug (11). Screening was carried out using 106 cpm per 137-mm filter under standard conditions (10).High molecular weight genomic DNA was digested with restriction endonucleases and blotted as described by Southern (14). For RNA blots, RNA was denatured in the presence of 50% (vol/vol) formamide and 2.2 M formaldehyde, subjected to electrophoresis on 1.2% agarose/formaldehyde gels, and blotted as described by Thomas (15). Final blot washing conditions were 0.1x SSC/0.1% NaDodSO4 at 500C. (lx SSC = 0.15 M NaCl/0.015 M sodium citrate, pH 7.0.)Restriction fragments from XMA5 and pMA34 inserts were subcloned into the M13mp8 vector and sequenced (16).The full-length cDNA insert from XMA5 was subcloned in the appropriate orientation in the EcoRI site of pSP65 (17). Trans...

show abstract

“…This appears as a low magnitude rise in Ca 2ϩ of short duration and most probably is due to the initial release of Ca 2ϩ from intracellular Ca 2ϩ stores ( Fig. 2A) (41,44,45).…”

Section: Cd2 Stimulation In the Absence Of P56 Lck Leads To A Prolongmentioning

confidence: 99%

“…In p56 lck expressing T cells, TCR stimulation is followed by an initial high transient Ca 2ϩ peak and a lower amplitude but sustained plateau phase (41,44,46). The initial rise of Ca 2ϩ is caused by the inositol trisphosphate-mediated release of Ca 2ϩ from the endoplasmatic reticulum (45) but is not sufficient for proliferation or IL-2 gene expression (41,71).…”

Section: Figmentioning

confidence: 99%

A p56 -independent Pathway of CD2 Signaling Involves Jun Kinase

Sunder‐Plaßmann

Reinherz

1998

Journal of Biological Chemistry

View full text Add to dashboard Cite

The p56lck Src family non-receptor tyrosine kinase has been shown to be critical for T lymphocyte differentiation and activation. Hence in the absence of p56 lck , T cell receptor triggered activation does not occur. We now provide evidence for a CD2-based signaling pathway which, in contrast to that of the T cell receptor, is independent of p56 lck . CD2-mediated interleukin-2 production occurs via activation of Jun kinase in cell lines lacking p56 lck . Jun kinase then facilitates the binding of c-Jun/c-Fos heterodimers to the AP-1 consensus site and the subsequent transcriptional activity of the interleukin-2 promoter. These data elucidate differences between TCR and CD2 signaling pathways in the same T cells.

show abstract

The T11 glycoprotein is functionally linked to a calcium channel in precursor and mature T-lineage cells.

Cited by 84 publications

References 20 publications

Bacterial toxins affect early events of T lymphocyte activation.

Bacterial toxins affect early events of T lymphocyte activation.

cDNA cloning and sequence of MAL, a hydrophobic protein associated with human T-cell differentiation.

A p56 -independent Pathway of CD2 Signaling Involves Jun Kinase

Contact Info

Product

Resources

About