scholarly journals The T Cell Receptor γ Chain Alternate Reading Frame Protein (TARP), a Prostate-specific Protein Localized in Mitochondria

2004 ◽  
Vol 279 (23) ◽  
pp. 24561-24568 ◽  
Author(s):  
Hiroshi Maeda ◽  
Satoshi Nagata ◽  
Curt D. Wolfgang ◽  
Gary L. Bratthauer ◽  
Tapan K. Bera ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Specific Protein ◽  
Reading Frame ◽  
Alternate Reading Frame Protein

scholarly journals Characterization of the Androgen-Regulated Prostate-Specific T Cell Receptor γ-Chain Alternate Reading Frame Protein (TARP) Promoter

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3433-3440 ◽  
Author(s):  
Wing-Shing Cheng ◽  
Valeria Giandomenico ◽  
Ira Pastan ◽  
Magnus Essand
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
T Cell ◽  
Cancer Cells ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Regulatory Sequence ◽  
Prostate Cancer Cells ◽  
Reading Frame ◽  
Alternate Reading Frame Protein

Abstract TARP (T cell receptor γ-chain alternate reading frame protein) is uniquely expressed in males in prostate epithelial cells and prostate cancer cells. Here we demonstrate that TARP expression is regulated by testosterone at the transcriptional level through specific binding of androgen receptor to an androgen response element in the proximal TARP promoter. We further demonstrate that the promoter specifically initiates reporter gene expression in TARP-positive prostate cancer cell lines. To develop a regulatory sequence for prostate-specific gene expression, we constructed a chimeric sequence consisting of the TARP promoter and the prostate-specific antigen (PSA) enhancer. We found that in the prostatic adenocarcinoma cell line LNCaP, the transcriptional activity of the regulatory sequence consisting of a TARP promoter and PSA enhancer is 20 times higher than the activity of a regulatory sequence consisting of the PSA promoter and PSA enhancer. Thus, our studies define a regulatory sequence that may be used to restrict expression of therapeutic genes to prostate cancer cells and may therefore play a role in prostate cancer gene therapy.

scholarly journals Molecular characterization of the feline T-cell receptor γ alternate reading frame protein (TARP) ortholog

2012 ◽  
Vol 13 (4) ◽  
pp. 345 ◽  
Author(s):  
Alexander Th. A. Weiss ◽  
Marie-Charlotte von Deetzen ◽  
Werner Hecht ◽  
Manfred Reinacher ◽  
Achim D. Gruber
Keyword(s):  
T Cell ◽  
Molecular Characterization ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Reading Frame ◽  
Alternate Reading Frame Protein

scholarly journals Differential association of protein tyrosine kinases with the T cell receptor is linked to the induction of anergy and its prevention by B7 family-mediated costimulation.

1996 ◽  
Vol 184 (2) ◽  
pp. 365-376 ◽  
Author(s):  
V A Boussiotis ◽  
D L Barber ◽  
B J Lee ◽  
J G Gribben ◽  
G J Freeman ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Kinase ◽  
Tyrosine Phosphorylation ◽  
T Cell Receptor ◽  
Tyrosine Kinases ◽  
Protein Tyrosine Kinase ◽  
Cell Receptor ◽  
Specific Protein ◽  
Protein Tyrosine ◽  
Potential Applications

When stimulated through their antigen receptor, without costimulation, T cells enter a state of antigen-specific unresponsiveness, termed anergy. B7-mediated costimulation, signaling via CD28, is sufficient to prevent the induction of anergy. Here we show that ligation of T cell receptor (TCR) by alloantigen alone, which results in anergy, activates tyrosine phosphorylation of TCR zeta and its association with fyn. In contrast, TCR ligation in the presence of B7 costimulation, which results in productive immunity, activates tyrosine phosphorylation of TCR zeta and CD3 chains, which associate with activated lck and zeta-associated protein (ZAP) 70. Under these conditions, CD28 associates with activated lck and TCR zeta. These data suggest that the induction of anergy is an active signaling process characterized by the association of TCR zeta and fyn. In addition, CD28-mediated costimulation may prevent the induction of anergy by facilitating the effective association of TCR zeta and CD3 epsilon with the critical protein tyrosine kinase lck, and the subsequent recruitment of ZAP-70. Strategies to inhibit or activate TCR-associated, specific protein tyrosine kinase-mediated pathways may provide a basis for drug development with potential applications in the fields of transplantation, autoimmunity, and tumor immunity.

scholarly journals Hybrid T cell receptor genes formed by interlocus recombination in normal and ataxia-telangiectasis lymphocytes.

1990 ◽  
Vol 172 (2) ◽  
pp. 409-418 ◽  
Author(s):  
S Lipkowitz ◽  
M H Stern ◽  
I R Kirsch
Keyword(s):  
T Cell ◽  
Sequence Analysis ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Open Reading Frame ◽  
Pcr Analysis ◽  
Constant Region ◽  
Hybrid Gene ◽  
Reading Frame ◽  
Hybrid Genes

In this paper, using polymerase chain reaction (PCR), we demonstrated the occurrence of hybrid genes formed by interlocus recombination between T cell receptor gamma (TCR-gamma) variable (V) regions and TCR-beta joining (J) regions in the peripheral blood lymphocytes (PBL) from normal individuals and patients with ataxia-telangiectasia (AT). Sequence analysis of the PCR-derived hybrid genes confirmed that site-specific V gamma-J beta recombination had occurred and showed that 10 of 23 genomic hybrid genes maintained a correct open reading frame. By dilution analysis, the frequency of these hybrid genes was 8 +/- 1/10(5) cells in normal PBL and 587 +/- 195/10(5) cells in AT PBL. These frequencies and the approximately 70-fold difference between the normal and AT samples are consistent with previous cytogenetic data examining the occurrence of an inversion of chromosome 7 in normal and AT PBL. We also demonstrated expression of these hybrid genes by PCR analysis of first-strand cDNA prepared from both normal and AT PBL. Sequence analysis of the PCR-amplified transcripts showed that, in contrast to the genomic hybrid genes, 19 of 22 expressed genes maintained a correct open reading frame at the V-J junction and correctly spliced the hybrid V-J exon to a TCR-beta constant region, thus allowing translation into a potentially functional hybrid TCR protein. Another type of hybrid TCR transcript was found in a which a rearranged TCR-gamma V-J exon was correctly spliced to a TCR-beta constant region. This form of hybrid gene may be formed by trans-splicing. These hybrid TCR genes may serve to increase the repertoire of the immune response. In addition, studies of their mechanism of formation and its misregulation in AT may provide insight into the nature of the chromosomal instability syndrome associated with AT. The mechanism underlying hybrid gene formation may be analogous to the mechanism underlying rearrangements between putative growth-affecting genes and the antigen receptor loci, which are associated with AT lymphocyte clones and lymphoid malignancies.

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