| 1. |
- Aas, AJ, et al.
(författare)
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Enhanced and quenched B(E1) transition rates between parity doublet bands in Ra-227
- 1996
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Ingår i: NUCLEAR PHYSICS A. - : ELSEVIER SCIENCE BV. - 0375-9474. ; 611:2-3, s. 281-314
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Tidskriftsartikel (refereegranskat)abstract
- The fast timing beta gamma gamma(t) method has been used to measure level lifetimes in the parity doublet bands in Ra-227 populated in the beta(-) decay of Fr-227. In particular, T-1/2 = 254(9) ps, 236(30) ps, less than or equal to 41 ps and 16(13) ps hav
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| 2. |
- Aas, AJ, et al.
(författare)
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Quenched E1 transition rates in Th-231
- 1999
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Ingår i: NUCLEAR PHYSICS A. - : ELSEVIER SCIENCE BV. - 0375-9474. ; 654:3-4, s. 499-522
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Tidskriftsartikel (refereegranskat)abstract
- The fast timing beta gamma gamma(t) method has been used to measure lifetimes of the low-lying levels in Th-231 populated in the beta(-) decay of Ac-231. The half-life of the K-pi = 5/2(-) band-head at 185.7-keV was measured as T-1/2 = 1073(79) ps, yieldi
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| 3. |
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| 4. |
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| 5. |
- Leusen, JHW, et al.
(författare)
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Disturbed interaction of p21-rac with mutated p67-phox causes chronic granulomatous disease
- 1996
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 184:4, s. 1243-1249
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Tidskriftsartikel (refereegranskat)abstract
- Chronic granulomatous disease (CGD) is characterized by the failure of phagocytic leukocytes to generate superoxide, needed for the intracellular killing of microorganisms. This is caused by mutations in any one of the four subunits of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In a rare, autosomal recessive form of CGD, a 67-kD cytosolic component of this enzyme (p67-phox) is missing. We here report on a patient with a mutation in the p67-phox gene that leads to expression of a nonfunctional p67-phox protein. The purified granulocytes of this patient failed to produce superoxide and contained about half of the normal amount of p67-phox. Analysis of the cDNA and genomic DNA of this patient showed that the patient is a compound heterozygote for a triplet nucleotide deletion in the p67-phox gene, predicting an in-frame deletion of lysine 58 in the p67-phox protein and a larger deletion of 11-13 kb in the other allele. Interestingly, the 58Lys deletion in p67-phox disrupts the interaction with p21-rac1, a ras-related protein involved in the activation of the NADPH oxidase. In contrast to normal neutrophils, in which p47-phox and p67-phox translocate to the plasma membrane upon cell activation, the cells of the patient did not show this translocation, indicating that an interaction between p67-phox and p21-rac1 is essential for translocation of these cytosolic proteins and activation of the NADPH oxidase. Moreover, this CGD patient represents the first case of disease caused by a disturbed binding of a ras-related protein to its target protein.
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| 6. |
- Mohamed, AJ, et al.
(författare)
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Signalling of Bruton's tyrosine kinase, Btk
- 1999
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Ingår i: Scandinavian journal of immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 49:2, s. 113-118
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Tidskriftsartikel (refereegranskat)
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| 7. |
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