Transcription expression

Northern blot analyses indicate that sequences of the four repeated elements are present on transcripts expressed in H. virescens by 2 hpp (25). Steady-state RNA levels peak at 2-6 hpp and then decline over the next 8 days. These transcripts are not as abundant as the cysteine-rich transcripts but are still major viral expression products. 

The glycosides forms of the isoflavones have a weaker estrogenic action compared with their aglycone counterparts. In fact, they bind weakly to both ERot and ERP and the receptor-dependent transcriptional expression is poor. Once the glucose molecule is removed, the isoflavones bind more strongly to the estrogen receptor (Morito et al., 2001). 

Bonaldo, M.F., Bair, T.B., Scheetz, T.E., et al. (2004) 1274 EuU-open reading frames of transcripts expressed in the developing mouse nervous system. Genome Res., 14, 2053-2063. 

The AhR is expressed in bone marrow stromal cells [14] and human hematopoietic stem cells [15] and upon agonist binding the receptor translocates to the nucleus, resulting in altered transcriptional expression such as increased CYPlAl [16] and resulting in reactive oxygen species [17]. Nonpharmaceutical compounds such as TCDD, benzo(a)pyrene and benzene have been shown to induce hematotoxicity using this mechanism in vivo and in vitro [18, 19]. 

Conventionally, the variants are characterized by coamplification with wild-type sequences using reverse transcription polymerase chain reaction (RT-PCR). However, this approach focuses on small regions of the known wild-type mRNA. Because of this threshold detection, spliced transcripts expressed at low levels may fall below the threshold of detection. To avoid this and other limitations of the conventional RT-PCR technique, the targeted amplification method can be used (Poola et al., 2000). This method involves the targeted amplification of the alternatively spliced molecules as separate gene populations using specific primers designed for the alternative splice junctions, without coamplification of wild-type molecules. 

Cortex Postmortem studies have, in addition to striatal expression, also focused on DA receptor expression in frontal and temporal cortices, with a few studies in the hippocampus and the thalamus ( Table 4.2-1). In cortex, abnormalities of transcript expression for D1( D2, and D5 have not been found in schizophrenia (Roberts et al., 1994 Meador-Woodruff et al., 1997). Two studies have found a decreased cortical expression of the D3 receptor transcript (Schmauss et al., 1993 Meador-Woodruff et al., 1997), while postmortem D4 receptor transcript expression was reported either decreased (Meador-Woodruff et al., 1997), increased (Stefanis et al., 1998), or unchanged (Mulcrone and Kerwin, 1996 Roberts et al., 1996). 

Several studies have analyzed the cortical expression of the NR1 subunit in postmortem brain ( Table 4.2-2). These studies report conflicting results, including both an increased and a decreased NR1 transcript expression in temporal cortex, OCC, and Dorsolateral prefrontal cortex, DLPFC (Humphries et al., 1996 Sokolov, 1998 Le Corre et al., 2000 Dracheva et al, 2001). However, other studies have reported unaltered NR1 transcript levels in PFC and temporal cortices (Akbarian et al., 1996 Beneyto et al., 2007). In addition, the expression of total NR1 protein in both frontal and temporal cortices was not significantly... 

The hippocampal expression of several PSD proteins was not significantly altered in schizophrenia, with the exception of a decreased PSD95 transcript expression in the molecular layer of the dentate gyrus, albeit only when compared with patients with major depression (Ohnuma et al., 2000a Toyooka et al., 2002 Toro and Deakin, 2005 McCullumsmith et al., 2007). Based on these studies, the expression in the hippocampus of the NMDA receptor complex does not appear profoundly affected in schizophrenia, although a few studies have reported modest regional changes of subunit expression (Harrison et al., 2003 Kristiansen et al., 2007). 

Clinton SM, Haroutunian V, Davis KL, Meador-Woodruff JH. 2003. Altered transcript expression of NMDA receptor-associated postsynaptic proteins in the thalamus of subjects with schizophrenia. Am J Psychiatry 160 1100-1109. 

McCullumsmith RE, Kristiansen LV, Beneyto M, Scarr E, Dean B, et al. 2007. Decreased NR1, NR2A, and SAP102 transcript expression in the hippocampus in bipolar disorder. Brain Res 1127 108-118. 

Meador-Woodruff JH, Haroutunian V, Powchik P, Davidson M, Davis KL, et al. 1997. Dopamine receptor transcript expression in striatum and prefrontal and occipital cortex. Focal abnormalities in orbitofrontal cortex in schizophrenia. Arch Gen Psychiatry 54 1089-1095. 

Yale, J. Bohnert, H. J. (2001). Transcript expression in Saccharomyces cerevisiae at high salinity. Journal of Biological Chemistry, 276, 15 996-6007. 

Hashimoto T, Bazmi HH, Mimics K, Wu Q, Sampson AR, Lewis DA. Conserved regional patterns of GABA-related transcript expression in the neocortex of subjects with schizophrenia. Am. J. Psychiatry 2008 165 479 89. 

Trapnell C, Roberts A, Goff L et al (2012) Differential gene and transcript expression analysis of RNA-seq experiments with TopHat and Cufflinks. Nat Protoc 7 562-578... 

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