Placental genes

Radaelli, T, Varastehpour, A.. Catalano, P and Hauguel-de Mouzon. S. (2003). Gestational diabete.s induces placental genes for chronic stress and inflammatory pathways. Diabetes 52,2951-2958. 

Page, N., Butlin, D., Manyonda, I., and Lowry, P., 2000, The development of a genetic profile of placental gene expression during the first trimester of pregnancy a potential tool for identifying novel secreted markers. Fetal Diagn Ther. 15 237-245. 

Chorionic Somatomammotropin. Three genes encode human chorionic somatomammotropin [11085-36-2] (hCS). These are located within a cluster of genes on human chromosome 17 which code for pituitary growth hormone [12629-01 -5] (GH-N), placental GH [109675-94-7J (GH-V), and three hCS molecules, ie, hCS-A, hCS-B, and hCS-V (1 3), also referred to as human placental lactogens. All of these molecules ate closely related to GH in stmcture (Fig. 1). Placental lactogens also exist in rodents and mminants however, these hormones are more closely related to prolactin than GH. 

Puromycin. Puromycin (19), elaborated by S. alboniger (1—4), inhibits protein synthesis by replacing aminoacyl-tRNA at the A-site of peptidyltransferase (48,49). Photosensitive analogues of (19) have been used to label the A-site proteins of peptidyltransferase and tRNA (30). Compound (19), and its carbocycHc analogue have been used to study the accumulation of glycoprotein-derived free sialooligosaccharides, accumulation of mRNA, methylase activity, enzyme transport, rat embryo development, the acceptor site of human placental 80S ribosomes, and gene expression in mammalian cells (51—60). 

Other gene mutations associated with placental development have been described that are not embryonic lethal but result in fetal growth retardation,... 

Finally, most of the imprinted genes known to date are expressed and imprinted in the placenta. Other imprinted genes are exclusively imprinted in the placenta but not in the fetus, and these may have a role specifically in placental growth or development (Engemann et al 2000). 

Wang, H., et al. Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. J. Biol. Chem. 1999, 274, 14875-14883. 

Fig. 9.2 Representative examples of the methylation-specific polymerase chain reaction (MSP) analyses for gene promoter regions. Lanes Lf and M indicate the presence of unmethylated and methylated template, respectively. Placental DNA (PDNA) and in vitro methylated DNA (IMD) served as negative and positive controls, respectively. Water (H) was used to detect contamination. Samples 1, 3, 4, and 7 indicate the presence of a methylated promoter DNA with various degrees of methylation, and samples 2, 5, and 6 represent an unmethylated promoter...

To obtain accurate results in qMSP/QM-MSP analyses, the best conditions have to be worked out to achieve reliable standard curves during the test trials. This could be achieved with the use of unmethylated and methylated templates such as placental DNA and in vitro methylated DNA, respectively, and by performing bisulfite treatment as described. To find the best condition for each gene, purify the DNA, calculate the concentration and copy numbers, and dilute the DNA sequentially (e.g., 1,1/2,1/4,1/8, 1/16, 1/32, and 1/64) and perform real-time PCR with several dilutions of the primers (e.g., 25, 50, 75ng each in various combinations). For example, you should see the amplification plots as indicated in Fig. 9.4 with 50% (Fig. 9.4A) or 25% (Fig. 9.4B) sequential dilution. These test trials and any other quantitative PCR (qPCR)ZQM-MSP experiments need to be done in duplicate or triplicate to ensure that the required skills and instruments for equal pipeting are in place, or the impacts could be minimized by averaging the results of the triplicate experiments. Similar to MSP, for each qMSP or QM-MSP trials use placental and... 

Stored under continuous light, and placental extracts from non-pungent fruit could synthesize capsaicinoids if vanillylamine and isocapric acid are provided. Together, these results raise the possibility that the gene product at Pml is a regulatory gene or a structural gene upstream in either the phenylpropanoid pathway or the branched chain fatty acid pathway and not capsaicinoid synthase. 

Screening for no-heat mutants in Capsicum collections and populations is a common practice for pepper breeders, as capsaicinoid accumulation is unique to the members of genus. A second locus for control of capsaicinoid production exists in at least two other species, C. chinense and C. chacoense [82], and the mutation that revealed this second locus is called loss of vesicle (Lov). The blisters on the placental surface that fill with capsaicinoids are absent in these no-heat mutants. The gene product and map location of this mutation are not known. 

Knockout of the prolactin receptor, rather than knockout of prolactin, is necessary to explore the role of the hormone and its receptor in maternal behavior because several molecules other than prolactin, including growth hormone (GH) and placental lactogens, may stimulate the prolactin receptor. Disruption of the prolactin receptor gene in a mouse model has allowed for assessment of phenotypes associated with partial and complete prolactin receptor deficits (Goffin et ah, 1999). Prolactin receptor knockout mice have severe reproductive deficits. Heterozygous mothers (receptor —/+) were also unable to lactate (Bridges, 1998). 

Berger J, Hauber J, Hauber R, Geiger R, Cullen BR (1988), Secreted placental alkaline phosphatase a powerful new quantitative indicator of gene expression in eukaryotic cells, Gene 66 1-10. 

Page, S. T., Owen, W. C., Price, K., and Elwood, P. C. (1993). Expression of the human placental folate receptor transcript is regulated in human tissues. Organization and full nucleotide sequence of the gene. ]. Mol. Biol. 229(4), 1175-1183. 

Twenty years ago, a high-affinity-binding site for uPA was demonstrated on the surface of peripheral blood monocytes and cultured cells of the human histiocytic lymphoma cell line, U937 [46]. The expression of uPAR on the cell surface of many cell types has since then been demonstrated, including a variety of neoplastic cell lines as well as nonneoplastic cells such as neutrophils, macrophages, keratinocytes, placental trophoblasts, endothelial, and smooth muscle cells [7, 33, 47-51]. The human uPAR gene has been mapped to chromosome 19ql.3 [52]. 

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