Disease relevance of ST5

• The candidate tumor suppressor genes WEE1, ST5, and rhombotin, are positioned on this map relative to these Beckwith-Wiedemann syndrome translocation and inversion breakpoints [1].
• Interestingly, the pediatric clone, isolated from most community-acquired infections in Cordoba, was characterized by ST100, a single-locus variant of ST5 and a new variant of SCCmec type related to SCCmec type IVc [2].
• In parallel, downregulation in ovarian cancer 1 (DOC1) and suppression of tumorigenicity (ST5) genes was observed, suggesting a potential increase for cancer development [3].
• ST-5 was probably introduced in Africa in 1987 and was responsible for most of the meningitis cases between 1988 and 2001 [4].

High impact information on ST5

• Evidence obtained with Tox2+ -unique and with random probes is consistent with a reciprocal translocation as the cause of the difference in the size of the HTS1-containing chromosome among the Tox2+ isolates studied here [5].
• We have isolated a chromosomal region, 22 kilobases (kb) long, that contains a 15.7-kb open reading frame (HTS1) encoding a multifunctional cyclic peptide synthetase [6].
• Expression of the human protein ST5-p70 correlates with reduced tumorigenic phenotype in mammalian cells, reverts their transformed phenotype, and restores their contact-dependent growth [7].
• Deletion of the COOH terminus converts the ST5 p70 protein from an inhibitor of RAS signaling to an activator with transforming activity in NIH-3T3 cells [7].
• Deletion of PR1 blocked the ability of p126 to activate ERK2 [8].

Biological context of ST5

• Based on these properties, we sought to investigate the activity of ST5 proteins in signal transduction pathways [8].
• In vitro, p126 displayed preferential binding to c-Abl SH3, as compared with other SH3 domains [8].
• These findings indicate that HTS1 represents a novel chromosome 11 gene which may be a target of the tumor suppressor gene active in this system [9].
• Chromosome localization studies mapped the HTS1 gene to chromosome 11p15, a region of chromosome 11 that is believed to contain a tumor suppressor gene [9].
• MLST revealed that 129/130 isolates had the same genotypes as internationally spread MRSA clones, including ST239, ST247, ST250, ST5, ST22, ST36, and ST8 [10].

Anatomical context of ST5

• Differential expression of the human ST5 gene in HeLa-fibroblast hybrid cell lines mediated by YY1: evidence that YY1 plays a part in tumor suppression [11].
• p126 (CDw101), a costimulatory molecule preferentially expressed on mucosal T lymphocytes [12].
• Recently, a feeder cell free-trophoblast cell line derived from Shiba-goat placenta, termed HTS-1, was established [13].
• Human leukocyte antigen class II control of the immune response to p126-derived amino terminal peptide from Plasmodium falciparum [14].
• A parasitophorous vacuole protein of Plasmodium falciparum, p126, is a potential candidate for a malaria vaccine [15].

Associations of ST5 with chemical compounds

• Whole cells of serotype b-specific polysaccharide antigen-defective mutants ST2 and ST5 were constructed by inserting transposon Tn916 into A. actinomycetemcomitans strain Y4 [16].
• The DNA sequence encodes tryptic peptides derived from two HC-toxin biosynthetic enzymes, HC-toxin synthetase 1 (HTS-1) and HC-toxin synthetase 2 (HTS-2), indicating that these two enzymes exist in vivo as part of a single polypeptide [17].
• Analysis of transcriptional control elements in the 5'-upstream region of ovine interferon-tau gene using feeder-independent caprine trophoblast cell line, HTS-1 [13].

Regulatory relationships of ST5

• Others, such as human MADD (MAP (Mitogen-activated protein) kinase activating protein containing death domain) and human ST5 (Suppressor of tumoreginicity 5) gene products are involved in regulation of MAPKs (Mitogen-activated protein kinases) signaling pathways [18].

Other interactions of ST5

• These observations suggest that ST5 can function as a signaling protein and can provide a link between c-Abl and ERK2 [8].
• The MRSA strains that were sequence type 8 (ST8), staphylococcal cassette chromosome mec (SCCmec) type IV, and Panton-Valentine leukocidin-positive clustered separately from those that were ST5 and SCCmec type II [19].

Analytical, diagnostic and therapeutic context of ST5

• All isolates had the same pulsed-field gel electrophoresis pattern, spaA type, and multilocus sequence type (MLST), which was identified as a single-locus variant of ST5, the MLST characteristic of previously characterized MRSA isolates with reduced susceptibility to vancomycin in the United States and Japan [20].
• Quantitative evaluation of the regulatory effects of divalent metal cations on the l-T3-sulfating activity of SULT1 ST5 revealed that Fe2+, Hg2+, Co2+, Zn2+, Cu2+, Cd2+ and Pb2+ exhibited dramatic inhibitory effects, whereas Mn2+ showed a significant stimulation [21].
• Molecular epidemiology of neisseria meningitidis isolated in the African Meningitis Belt between 1988 and 2003 shows dominance of sequence type 5 (ST-5) and ST-11 complexes [4].
• By electrophoretic mobility shift assay, a nuclear protein from HTS-1 cells was confirmed to bind specifically to the Ets-2 site of oIFNtau promoter region [13].

References