ライフサイエンスコーパス: Nesp

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1 d two oppositely imprinted genes, Gnasxl and Nesp.

2 ion-time curve was significantly greater for NESP (291.0 +/- 7.6 ng x h per ml versus 131.9 +/- 8.3 n

3 The volume of distribution was similar for NESP and Epoetin (52.4 +/- 2.0 ml/kg versus 48.7 +/-2.1

4 Nesp and Gnasxl represent oppositely imprinted promoters

5 the Nesp-Gnasxl-Gnas region was determined: Nesp and Gnasxl were found to be 15 kb apart, and Gnasxl

6 of the NESP55 and XLalphas promoter regions (Nesp and Gnasxl) is not established during gametogenesis

7 -regulation of Nespas and down-regulation of Nesp and Gnasxl.

8 The upstream Nesp and Nespas/Gnasxl promoters are paternally and mate

9 ins closely juxtaposed maternally expressed (Nesp) and paternally expressed (Nespas, Gnasxl, Exon 1A)

10 Remarkably, Gnasxl, Nesp, and Gnas are all part of the same transcription un

11 5 promoter region, the maternally methylated NESP antisense (NESPAS)/XLalphas promoter region and the

12 anscription unit; transcripts for Gnasxl and Nesp are alternatively spliced onto exon 2 of Gnas.

13 We show that Epo and NESP are degraded only by cultured cells that express th

14 Surface-bound Epo and NESP are internalized at the same rate (k(in) = 0.06 min

15 ion explains why Epo is degraded faster than NESP at the cellular level.

16 he novel erythropoiesis-stimulating protein (NESP) bring new options to allogeneic blood transfusion.

17 d the trafficking and degradation of Epo and NESP by EpoR-expressing cells.

18 acokinetics of an equivalent peptide mass of NESP by subcutaneous injection in six of these patients.

19 associated with the trans-Golgi network and Nesp encodes a secreted protein of neuroendocrine tissue

20 ted transcripts were up-regulated, including Nesp, Gnasxl and Exon1A.

21 Imprinting of alternative transcripts, Nesp, Gnasxl and Nespas, in the cluster is unaffected.

22 ized into six transcriptional units, Nespas, Nesp, Gnasxl, F7, exon 1A, and Gnas.

23 The organization of the Nesp-Gnasxl-Gnas region was determined: Nesp and Gnasxl

24 ed novel erythropoiesis-stimulating protein (NESP), has a lower affinity than Epo for the EpoR but ha

25 The longer half-life of NESP is likely to confer a clinical advantage over Epoet

26 odes a paternal-specific transcript, whereas Nesp is paternally methylated with maternal-specific exp

27 Novel erythropoiesis stimulating protein (NESP) is a hyperglycosylated analogue of recombinant hum

28 Epo binds surface EpoR faster than NESP (k(on) = 5.0 x 10(8) m(-1) min(-1) versus 1.1 x 10(

29 lation: paternal-specific methylation at the Nesp locus and maternal-specific methylation at the Gnas

30 inted transcripts in the mouse Gnas cluster (Nesp, Nespas, Gnasxl, Exon 1A and Gnas) provides a model

31 ethylate maternal imprint marks) showed that Nesp, Nespas/Gnasxl, and 1A imprinting depend on one or

32 These mice had normal Nesp-Nespas/Gnasxl imprinting, indicating that the Gnas

33 ciated with the three genotypes based on the NESP:/NESPAS: sense/antisense and GNASXL: transcripts in

34 Our kinetic model of Epo and NESP receptor binding, intracellular trafficking, and de

35 The mean terminal half-life for subcutaneous NESP was 48.8 h.

36 The peak concentration of subcutaneous NESP was approximately 10% of that following intravenous

37 The mean terminal half-life for intravenous NESP was threefold longer than for intravenous Epoetin (

38 (100 U/kg) and an equivalent peptide mass of NESP were compared following intravenous bolus in 11 sta

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