ライフサイエンスコーパス: X-SCID

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1 X-SCID, the most common form of human SCID, is due to mu

2 rr virus-transformed cell line (LCL) from an X-SCID patient with a gamma-c null mutation.

3 arising as secondary, adverse effects in an X-SCID gene therapy trial.

4 opriate IL-2R function can be restored in an X-SCID LCL by transduction of a wild-type gamma-c gene.

5 cells, confirming correction of the cellular X-SCID phenotype.

6 X-linked severe combined immune deficiency (X-SCID) in gene-therapy trials using haematopoietic stem

7 d severe combined immunodeficiency diseases (X-SCID).

8 d severe combined immunodeficiency disorder (X-SCID) suggests that we might now be at the point where

9 Gene-therapy trials for X-SCID, which have been based on the assumption that IL2

10 iral vector insertions in T-cell tumors from X-SCID patients in gene therapy trials.

11 unological defects that are similar to human X-SCID.

12 h X-linked severe combined immunodeficiency (X-SCID) are deficient in gammac and provide a useful mod

13 r X-linked severe combined immunodeficiency (X-SCID) has prompted safety concerns.

14 r X-linked severe combined immunodeficiency (X-SCID) have led to a re-evaluation of risks following g

15 X-linked severe combined immunodeficiency (X-SCID) is an immune disorder caused by mutations in the

16 e X-linked severe combined immunodeficiency (X-SCID).

17 e downstream signalling through the IL-2R in X-SCID cell lines, suggesting that gene therapy may be a

18 phosphorylation and DNA binding activity in X-SCID B cells with a wide range of gammac mutations.

19 rentiation at the T cell progenitor stage in X-SCID cells.

20 Here I argue that in X-SCID it is the parents and children whom we should lis

21 To model X-SCID in vitro, we generated a mouse embryonic stem cel

22 ypothesis that the molecular pathogenesis of X-SCID is due primarily to gamma(c)-mediated defects in

23 re proposed to cause the severe phenotype of X-SCID patients.

24 We found that although IL-4 stimulation of X-SCID B cells did not result in Janus tyrosine kinase-3

25 Using a mouse model for gene therapy of X-SCID, we find that the corrective therapeutic gene IL2

26 The X-SCID background in transplanted cells was required for

27 However, reconstitution of these X-SCID B cells with gammac enhanced IL-4-mediated respon

28 Transduced X-SCID LCL expressed the G1gamma-cSvNa transcript.

29 can also occur in T-cell receptor-transgenic X SCID mice lacking HSV-specific T cells.

30 ctor integration in one of the patients with X-SCID.

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