Disease relevance of SART1

• Expression of the SART1 tumor-rejection antigen in human osteosarcomas [1].
• Expression of the SART1 tumor-rejection antigens in colorectal cancers [2].
• We have previously described the SART1 gene, which encodes both the SART1(259) antigen expressed in the cytosol of the majority of squamous cell carcinomas and some adenocarcinomas and the SART1(800) antigen expressed in the nucleus of the majority of proliferating cells [3].
• Expression of the SART1 tumor rejection antigen in renal cell carcinoma [3].
• Expression of the tumor-rejection antigen SART1 in brain tumors [4].

Psychiatry related information on SART1

• We also show that errors (false presses) on the SART can be predicted by a significant shortening of reaction times in the immediately preceding responses, supporting the view that these errors are a result of 'drift' of controlled processing into automatic responding consequent on impaired sustained attention to task [5].

High impact information on SART1

• In this paper, we describe the chromosomal localization of the gene for squamous cell carcinoma-associated reactive antigen for cytotoxic T cells (SART-1) [6].
• We therefore hypothesize that polymorphic variation within the SART-1 gene may account for individuals developing atopy [6].
• SART1 and heterogeneous nuclear RNP M were both shown to be genuine SUMO targets, confirming the validity of the approach [7].
• Both the U5-specific, TPR/HAT-repeat-containing hPrp6 protein and the tri-snRNP-specific hSnu66 protein interact with several U5- and U4/U6-associated proteins, including hBrr2 and hPrp3, which contacts the U6 snRNA [8].
• HLA-A24-restricted and SART1-specific CTLs recognized the HLA-A24+ and SART1(259)+ glioma cells, and the levels of recognition correlated both with HLA-A24-antigen expression level and with the concentration of the SART1 peptide antigen [4].

Biological context of SART1

• Cytokines required for induction of histocompatibility leukocyte antigen-class I-restricted and tumor-specific cytotoxic T lymphocytes by a SART1-derived peptide [9].
• Western blot analysis confirmed that the apoptosis pathway was activated by SART-1 gene transduction [10].
• Cell cycle arrest and apoptosis induced by SART-1 gene transduction [10].
• The biological function of the SART-1 gene product is demonstrated and its potential as a target for cancer gene therapy is discussed [10].
• Cell count analysis using Trypan-Blue dye exclusion showed that SART-1 gene transduction inhibited cell growth [10].

Anatomical context of SART1

• The cancer cell lines were tested for their ability to stimulate interferon-gamma production by the human-leukocyte-antigen-A24-restricted and SART1-specific cytotoxic T lymphocytes and were also tested for their susceptibility to the lysis by the cytotoxic T lymphocytes [2].
• METHODS: SART1 antigens were investigated by Western blotting in six colorectal cancer cell lines and in 33 colorectal cancer tissues [2].
• This temperature sensitivity could be suppressed by overproduction of Rpb10 or Snu66, the former of which is one of the common subunits of the RNA polymerases and the other is the component of the spliceosome [11].
• Generation of a human leukocyte antigen-A24-restricted antitumor cell with the use of SART-1 peptide and dendritic cells in patients with malignant brain tumors [12].

Associations of SART1 with chemical compounds

• We have also developed a new L-shaped titanium plate (HOMS Engineering Inc., Nagano, Japan) that fits into the fixation unit [13].
• Lidocaine had no consistent effects on sinus rate, SART, atrial refractoriness, or A-V nodal conduction as measured by pooled AH intervals and the Wenckebach point, and on A-V nodal refractoriness [14].
• In particular, retardation of absorbance increase at 234 nm as formation of the conjugated diene hydroperoxides in a real pork oil system stored at 60 degrees C, supplement of Ara-1 at 100 microM has shown equivalent or even greater activity than did BHT [15].
• During incubation of the peanut slices, contents of Res, Ara-1, and Ara-3 increased tremendously from initially trace or not detectable amounts up to 147.3, 495.7, and 2414.8 microg/g, corresponding to 20, 16, and 24 h of incubation, while IPD contents continued to increase up to 28 h (4474.4 microg/g) [15].

Other interactions of SART1

• The human-lymphocyte-antigen-A24-restricted and SART1-specific cytotoxic T lymphocytes killed the human-lymphocyte-antigen-A24+ SART1(259+) cancer cells [2].
• They included SART1, p57Kip2, ROCK-1, gamma-catenin, and heat shock proteins, which are classified as tumor-associated genes [16].
• The HLA-A2-restricted CTL recognized the SART-1, but not the MAGE-1 or MAGE-3 antigen [17].

Analytical, diagnostic and therapeutic context of SART1

• Therefore, the SART1 peptide could be an appropriate molecule for use in peptide-based specific immunotherapy for RCC patients [3].
• SART1 was confirmed by immunoblotting to have both SUMO-1- and SUMO-2-linked forms at similar levels [18].
• In addition, SART-1 is known to be a tumor antigen in a range of cancers recognized by T cells, thus a potential strategy would be the combination of suicide gene therapy with immuno-gene therapy [10].
• Flow cytometry analysis suggested that SART-1 gene transduction induced cell cycle arrest followed by apoptosis [10].
• We also report a highly significant correlation of -0.58 between SART performance and Glasgow Coma Scale Scores in the TBI group [5].

References