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Junction sequence

Lafaille, J.J., DeCloux, A., Bonneville, M., Takagaki, Y., Tonegawa, S. (1989). Junctional sequences of T cell receptor y genes implications for yd T cell lineages and for a novel intermediate of V-(D)-J joining. Cell 59,859-870. [Pg.80]

Victor, K.D., Vu, K., Feeney, A.J. (1994). Limited junctional diversity in K light chains. Junctional sequences from CD43+B220+ early B cell progenitors resemble those from peripheral B cells. J. Immunol. 152,3467-3475. [Pg.93]

The MCS is a stretch of unique restriction endonuclease cleavage sites between the promoter and the poly (A) signal in expression plasmid vectors, and is used as a common area to insert a cDNA or gene of interest. By using the MCS, the genes of interest can be inserted and assayed with ease. Sticky-end and blunt-end vector strands are available at different restriction sites. Although the MCS is very convenient, it should be noted that these sites usually remain in the mRNA transcribed from the expression unit of the vector and may reduce its stability or the efficiency of translation. Furthermore, one must be careful not to produce an ATG codon at the junctional sequence between the MCS and the insert, because it may work as a false start codon in the resulting mRNA and interfere with the production of the correct product. [Pg.8]

Mount SM. A catalogue of splice junction sequences. Nucleic Acids Res. 1982 10 459-472. [Pg.1680]

Bipolar junction transistors are based on an n-p-n or p-n-p junction sequence. One of the p-n junctions is reverse biased, which suppresses the current between the outer electrodes, commonly called emitter and collector. The middle layer, which is connected to a third electrode (base), is spatially very thin. Initiated by a small control current over the base electrode, charge carriers are injected over the forward biased p-n junction and minority carriers can flood directly over the reverse biased p-n junction. This causes an increased current between emitter and collector. In contrast to FETs, bipolar junction transistors are current controlled. [Pg.513]

Some types of -thalassemia (little or none of the hemoglobin p chain produced) are caused by homozygous mutations in the splice junction sequences at intron/exon boundaries. In some individuals, an AT replaces a GT in the gene at the 5 end of the first or second intron. Mutations also occur within the splice junction sequences at the 3 -end of introns (GT at the donor site 5 -end and AG at the acceptor site 3 -end). Mutations at either site totally abolish normal splicing and result in p thalassemia. [Pg.248]

Ehrenstein, M. R., Rada, C., Jones, A. M., Milstein, C., and Neuberger, M. S. (2001). Switch junction sequences in PMS2-deficient mice reveal a microhomology-mediated mechanism of Ig class switch recombination. Proc. Natl. Acad. Set. USA 98, 14553-14558. [Pg.329]

Osheim. Y. N., Miller, O. L Jr., and Beyer, A. L. (1985). RNP particles at splice junction sequences on Drosophila chorion transcripts. Cell (Cambridge, Mass.) 43,143-151. [Pg.496]

These are plasmids resulting from the pBIlOl construction that provide the other two reading frames of GUS relative to the polylinker sites. Junction sequences of the pBIlOl series, with the pUC19 polylinker sequence followed by the GUS coding sequence, is as follows the GUS initiator is boldface, the BamHI site is underlined ... [Pg.261]

Bipolar transistors are realized using either an npn- or pnp-junction sequence. The different segments of the device are named as collector, base, and emitter electrode, respectively. In order to operate the transistor, one of the junctions is forward biased, while the other is biased in reverse. Using a small control current over the base electrode, a significant current between the collector and emitter electrodes is enabled. [Pg.214]

In some cytogenetic abnormalities, such as certain leukemias, chimeric fusion mRNAs connecting strange exons result from reciprocal chromosomal translocations and cause abnormalities. For the design of ribozymes that can disrupt such chimeric RNAs, it is necessary to target the junction sequence. Otherwise, normal mRNAs that share part ofthe chimeric RNA sequence will also be cleaved by the ribozyme, with resultant damage to the host cells. [Pg.429]


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