Disease relevance of PSG5

• Pregnancy-specific beta 1 glycoprotein genes (PSG) are mainly expressed during human placental development, though their expression has been reported in other normal and pathological tissues, e.g. hydatidiform mole (HM), of distinct origins [1].
• To study the molecular mechanisms that regulate expression of the PSG gene, we established a human amnion cell line, HAA58OD-8C, immortalized with an origin-defective simian virus-40 (SV40) temperature-sensitive A58 mutant virus [2].
• We conclude that PSG within a few days following UPPP is warranted in patients with obstructive sleep-disordered breathing to determine if there has been worsening of upper airway function or oxygenation (or both) during sleep in the early postoperative period [3].
• PSG genes showing different patterns of expression were expressed in baculovirus, and the purified proteins examined for their effects on cytokine expression [4].
• Appearance of Lf in the ductal cells of PSG indicates an early sign of palatal sialadenitis [5].

Psychiatry related information on PSG5

• When comparing a 16-channel PSG montage with that of a seven-channel cardiorespiratory montage, we found that 84% of all movement/arousals could be detected using the abbreviated montage [6].
• Although the 1995 practice parameters paper determined that actigraphy was not appropriate for the diagnosis of sleep disorders, more recent studies suggest that for some disorders, actigraphy may be more practical than PSG [7].
• Few sleep laboratories have PSG equipment that allows for the recording of 18 channels of EEG without compromising the ability to detect sleep apnea, periodic limb movements, and parasomnias [8].
• Each PSG recording was blindly scored using conventional scoring criteria, and resulting measures of total sleep period, total sleep time, sleep efficiency percent, stage 1 time, slow-wave sleep time, and rapid eye movement latency were used to compare the two subject groups within each PSG recording site (i.e. lab and home) [9].
• Effects of reviewing DATATOP videotapes on IQ and MMPI in PSG coordinators and investigators, or, whatever happened to Tony Lang [10]?

High impact information on PSG5

• Members of the human and murine PSG family induce secretion of antiinflammatory cytokines in mononuclear phagocytes [11].
• One-quarter of these patients had dyspnea, chest pain, or syncope combined with electrocardiographic left ventricular hypertrophy (LVH) and strain, and these all had peak LV outflow gradients (PSG) greater than 85 mm Hg [12].
• Eleven pregnancy-specific glycoprotein (PSG) genes reside on human chromosome 19 [13].
• In transient transfection assays using a chloramphenicol acetyltransferase reporter gene, we demonstrated that the -835 to -34 DNA region upstream of the translation start site of PSG12 or PSG12 psi contained both positive and negative elements that control PSG expression [14].
• The PSG proteins share 85-95% sequence homology in the coding region, but show variability at the carboxyl-terminal (COOH) domains [15].

Biological context of PSG5

• We show in transient transfection experiments performed in HeLa, COS-7 and JEG-3 cells, that such mutation completely abolished the transcriptional activity of the PSG5 promoter, independently of the cell type [1].
• We have estimated the size of the PSG subfamily by identification of N-domain exons from isolated genomic clones and from total genomic DNA through PCR amplification and DNA sequence determination [16].
• Here we report the cloning of four cDNAs coding for different members of the PSG family from a human fetal liver cDNA library [17].
• 2. Using a high-resolution restriction fragment fingerprinting technique, we have assembled 256 cosmids from the PSG region into a single 700-kb contig [18].
• The recovery of platelet count after bone marrow transplant was much faster in mice receiving 1 microg PSG/day than in animals in any other group [19].

Anatomical context of PSG5

• Our results indicate that the cis-acting and trans-acting elements analyzed are indispensable to support PSG5 promoter activity in cell lines which do or do not produce PSG [1].
• Both type I and type II transcripts of the PSG genes were detected in blood cells with the exception of type II transcript of PSG5 and PSG11 which were only found in the placenta [20].
• The human pregnancy-specific glycoprotein (PSG) family consists of eleven closely related molecules mainly synthesized by placental syncytiotrophoblasts and whose function(s) are unknown [21].
• The PSG-5', PSG93-specific, PSG16/PSG93-3', and PSG95-3' probes, which identify the majority of PS beta G mRNAs, hybridized with three PS beta G mRNAs of 2.3, 2.2, and 1.7 kilobases from placental fibroblasts [22].
• Trace amounts of PSG transcripts could be detected in polymorphonuclear cells (PMN), monocytes and B lymphocytes while T lymphocytes always contained the highest level of transcript [20].

Associations of PSG5 with chemical compounds

• Moreover, PSG expression was greatly induced by 5-bromo-2'-deoxyuridine (BudR), which selectively increased synthesis of PSGs of 72 and 54 kDa [23].
• The members of the carcinoembryonic antigen (CEA)/pregnancy-specific glycoprotein (PSG) gene family have a characteristic N-terminal domain that is homologous to the immunoglobulin variable region [16].
• Sodium butyrate, an inducer of PSG synthesis, greatly stimulated expression of all PSG1-I-chloramphenicol acetyltransferase (CAT) fusion gene constructs [24].
• PSG9 and PSG10 are representatives of two distinct classes of PSG protein that have N-termini with or without the Arg-Gly-Asp motif implicated in adhesion [25].
• From the PSG antiserum, antibodies can be isolated that differentially bind to V-like PSG domains which differ by eight non-conservative amino acid substitutions, three of which are clustered in a position corresponding to the CDR III of immunoglobulin V region domains [26].

Physical interactions of PSG5

• It was previously demonstrated that Krüppel-like factor 6 (KLF6) and specific-protein 1 (Sp1) bind to conserved sequence within the PSG-5 gene promoter [27].

Other interactions of PSG5

• BudR stimulated the expression of all PSG transcripts except PSG4 [23].
• Ribonuclease protection analysis showed that butyrate increased the PS beta G mRNAs containing the PSG-5' or PSG93-specific sequence to approximately 20% of human placental levels [22].
• To characterize PSG promoter activity, we constructed chloramphenicol acetyltransferase (CAT) fusion genes containing -809 to -44 basepairs up-stream of the translational start site of the PSG6 gene [28].
• We describe the isolation and characterization of two additional PSG cDNAs, PSG9 and PSG10, whose transcripts are largely expressed in placental tissue and to a lesser extent in some other cell types, including myeloid cells differentiated to granulocytes [25].
• Seven novel genes (CGM12 to CGM18) were found in the PSG region [29].

Analytical, diagnostic and therapeutic context of PSG5

• Detailed restriction mapping and hybridization with gene-specific probes indicated that the order of the 11 Previously identified PSG genes is cen-PSG3-PSG8-PSG12-PSG1-PSG6-PSG7-+ ++PSG13-PSG2-PSG5-PSG4-PSG11-tel [18].
• In situ hybridization analyses of metaphase chromosomes reveal that all the human pregnancy-specific glycoprotein (PSG) genes are located on the long arm of chromosome 19 (19q13.2-13.3), overlapping the region containing the closely-related carcinoembryonic antigen (CEA) gene subgroup [30].
• RNA isolated from bone marrow and peripheral blood cells of healthy individuals was analyzed for PSG transcripts by reverse transcriptase-polymerase chain reaction using synthetic oligonucleotide primers specific for the PSG genes [20].
• Cytokine production in response to PSG-treatment was measured by ELISA and/or reverse transcriptase-PCR [31].
• Except for a stronger hybridization signal obtained at 9 weeks of gestation, which might be correlated to the development of the placenta, the relative amounts of the different PSG mRNAs showed little variation throughout pregnancy as revealed by Northern blots performed at 6, 13, 18 and 40 weeks of gestation [32].

References