Disease relevance of SULT4A1

• Integrated genomic and expression profiling allowed us to identify genes of which the expression is deregulated in intracranial ependymoma, such as overexpression of the putative proto-oncogene YAP1 (located at 11q22) and downregulation of the SULT4A1 gene (at 22q13.3) [1].
• The hBR-STL and rBR-STL cDNAs were expressed in both Escherichia coli and Sf9 insect cells in the presence or absence of an N-terminal histidine-affinity tag (His-tag) [2].
• The recovery of circulating antigen-specific T-cell immunity to Epstein-Barr virus (EBV) was determined in ELIspot assays following allogeneic myeloablative or nonmyeloablative stem cell transplantation (MST/NST) [3].
• Cx26 was up-regulated in the carcinoma cells of 15 of the 27 invasive NST carcinomas, although the staining was usually cytoplasmic and heterogeneous [4].
• Since accumulating evidence suggests that ductal carcinoma of no special type (NST) represents a diverse group of biologies, this study has focused on grade III ductal carcinoma, in order to reduce the heterogeneity of the study population [5].

Psychiatry related information on SULT4A1

• Moderate users performed significantly better than heavy users; there were no significant psychomotor performance differences comparing ST/NST conditions [6].

High impact information on SULT4A1

• When the patients were returned to ambient air breathing, a mean of 13% increase of sigmaST and 19% of NST from the levels recorded during oxygen inhalation were observed [7].
• In contrast, only 1 of 9 (95% confidence interval [CI], 0-2.8) patients made a detectable EBV-specific response by 6 months following NST conditioned with fludarabine, melphalan, and alemtuzumab [3].
• Conversion to full donor myeloid chimerism following NST occurred significantly sooner in cases with, compared with cases without, PRCA (30 versus 98 days; P =.008) [8].
• To evaluate these events following reduced-intensity nonmyeloablative SCT (NST), consecutive series of patients with major ABO incompatibility undergoing either NST (fludarabine/cyclophosphamide conditioning) or myeloablative SCT (cyclophosphamide/high-dose total body irradiation) were compared [8].
• These data indicate that significantly delayed donor erythropoiesis is (1) common following major ABO-incompatible NST and (2) associated with prolonged persistence of host antidonor isohemagglutinins [8].

Biological context of SULT4A1

• The hBR-STL-1 cDNA contains an 852-nt open reading frame encoding a 284-amino-acid protein with a calculated molecular mass of 33083 Da [2].
• This segment of chromosome 22 contains the sulfotransferase-4A1 (Sult4A1) gene, which encodes an enzyme thought to be involved in neurotransmitter metabolism in the central nervous system [9].
• Donor red blood cell (RBC) chimerism (initial detection of donor RBCs in peripheral blood) was markedly delayed following NST versus myeloablative SCT (median, 114 versus 40 days; P <.0001) and strongly correlated with decreasing host antidonor isohemagglutinin levels [8].
• Hence, two measures of differentiation can be compared for a single data set: one (GST) that makes use only of the allelic frequencies and the other (NST) for which similarities between the haplotypes are taken into account in addition [10].
• Patients with less than 90% of donor T cells 4 weeks after NST had a significantly higher risk of relapse, graft rejection, or both (14 of 18 patients) than patients with donor T-cell chimerism of 90% and higher (3 of 20 patients) [11].

Anatomical context of SULT4A1

• Polyclonal antibodies were raised in chickens against purified His-tagged hBR-STL, and were used to detect the presence of rBR-STL in adult male and female rat brain cytosol [2].
• Cx43 was expressed by stromal cells, possibly myofibroblasts, in all NST carcinomas [4].
• Non-myeloablative stem cell transplantation (NST): chimerism testing as guidance for immune-therapeutic manipulations [12].
• METHODS: We quantified donor long-term culture-initiating cells (LTC-IC) in nine patients during the early phase after NST and lineage-specific donor cells of myeloid (CD33+, CD34+, granulocytes) and lymphoid lineage (CD3+, CD4+, CD8+, CD56+) in 38 patients with a median follow-up of 40 weeks after NST [11].
• Outside the NST, cells in the spinal trigeminal nucleus and parvicellular reticular formation were also labelled after PBN injections [13].

Associations of SULT4A1 with chemical compounds

• Cyclosporine withdrawal appeared to induce graft-mediated immune effects against recipient isohemagglutinin-producing cells, resulting in decreased antidonor isohemagglutinin levels and resolution of PRCA following NST [8].
• Relative to an NST strategy, alendronate has a fairly good cost-effectiveness ratio [14].
• Here we show that responses to taste stimulation recorded extracellularly from NST cells in vivo can be inhibited by local microinjections of GABA; this inhibition is blocked by the GABAA receptor antagonist bicuculline methiodide [15].
• The effect of an intravenous maternal glucose load upon fetal activity and FHR was studied 51 times in 48 pregnancies at 34 or more weeks, in which the fetuses were classified as non-reactive during the NST [16].
• After 24 h there was a fall in NST of 45% (71% with nitroglycerin and 145% in the control group); after 48 h there was a 41% decrease (compared with 65% in the nitroglycerin group and 142% in the control group) [17].

Other interactions of SULT4A1

• Localization of a brain sulfotransferase, SULT4A1, in the human and rat brain: an immunohistochemical study [18].

Analytical, diagnostic and therapeutic context of SULT4A1

• Northern-blot analyses of RNA isolated from eight human tissues indicate that the hBR-STL message is selectively expressed in brain [2].
• Parallel surveillance demonstrated that other virus infections occurred more frequently and earlier after transplantation in NST patients [3].
• Interestingly, all LTC-IC were from donor origin 2 and 4 weeks after NST, but rapid establishment of donor LTC-IC was not predictive for progression-free survival [11].
• The difference between NST and GST can be caused by several factors, including sampling artefacts, unequal effect of mutation rates and phylogeographic structure [10].
• Exposure of gold surfaces to solutions of dithiobis N-succinimidyl propionate (DTSP) gives rise to the modification of the surface with N-succinimidyl-3-thiopropionate (NSTP) which can, in turn, react with amino groups allowing for the covalent immobilization of enzymes such as horseradish peroxidase (HRP) [19].

References