| 1. |
- Dunham, I, et al.
(författare)
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The DNA sequence of human chromosome 22
- 1999
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 402:6761, s. 489-495
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Liu, K, et al.
(författare)
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Temporal expression of urokinase type plasminogen activator, tissue type plasminogen activator, plasminogen activator inhibitor type 1 in rhesus monkey corpus luteum during the luteal maintenance and regression.
- 1997
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Ingår i: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 133:2, s. 109-16
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Tidskriftsartikel (refereegranskat)abstract
- Proteolytic activity generated by the plasminogen activator (PA) system has been associated with many biological processes. Using a pregnant mare serum gonadotropin (PMSG)/human chorionic gonadotropin (hCG)-induced rhesus monkey corpus luteum (CL) model, we have studied how urokinase-type plasminogen activator (uPA), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor type 1 (PAI-1), are temporally expressed in CL of rhesus monkey at the luteotropic and luteolytic periods. Slot blot analysis and in situ hybridization were performed to analyze the expression and distribution of uPA and PAI-1 messenger RNA (mRNA). Fibrin overlay was used to detect uPA and tPA activities. We found that uPA is the dominating PA in luteotropic CL in the monkey. Abundant expression of PAI-1 mRNA was detected. The highest expression of uPA and PAI-1 mRNA was observed at the luteotropic period, while their expression decreased approximately 50% at early luteal regression defined by considerably decreased serum progesterone levels, and remained at very low levels at the late stage of luteal regression. We also observed an increased tPA activity at the time of luteal regression. Moreover, the exogenous tPA could inhibit the progesterone production in cultured luteal cells from 13-day-old monkey CL. We also used LH receptor mRNA expression as a mark for the luteal phases. A highly expressed, evenly distributed LH receptor mRNA was detected in CL during the luteotropic phase, while its expression decreased at day 13 coinciding with the reduction of progesterone production. We conclude that proteolysis mediated by uPA and regulated by PAI-1 may play a role in the luteal maintenance, while tPA may participate in the luteal regression in the rhesus monkey.
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| 3. |
- Liu, Y X, et al.
(författare)
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Prolactin regulation of tissue type plasminogen activator and plasminogen activator inhibitor type-I gene expression in eCG-primed rat granulosa cells in culture.
- 1998
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Ingår i: Biology of Reproduction. - 0006-3363 .- 1529-7268. ; 59:2, s. 409-16
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Tidskriftsartikel (refereegranskat)abstract
- The present study was designed to investigate the effect of prolactin (PRL) on plasminogen activator inhibitor-I (PAI-I) and tissue type plasminogen activator (tPA) gene expression in eCG-primed granulosa cells in vitro. At 46 h after the hormone treatment, ovaries were removed, and granulosa cells were prepared for culture. Cells were incubated for various times in serum-free medium in the presence or absence of LH and PRL alone or in combination. tPA and PAI-I activities in the media were assayed by fibrin overlay and reverse fibrin autograph, respectively. Cytoplasmic RNA from granulosa cells was prepared using the NP-40 method and was assayed for PAI-I and tPA mRNA levels. We demonstrated the following. 1) PRL increased PAI-I mRNA production in cultured granulosa cells. Inclusion of LH with PRL had a synergistic effect on increasing PAI-I mRNA levels. After 48-h culture, 3-fold increases in PAI-I mRNA levels were seen with LH in combination with PRL as compared with PRL alone. The synergistic increase in PAI-I mRNA levels occurred in a dose- and time-dependent manner. 2) The increase in PAI-I mRNA synthesis by PRL alone, or by PRL in combination with LH, was well correlated with the changes in PAI-I activity and antigen levels in the conditioned media. 3) PRL in the culture also dramatically decreased LH-induced tPA mRNA and activity in a dose- and time-dependent fashion. The decrease in the tPA activity by PRL was also correlated with an increase in the amount of PA-PAI-I complexes in the cell-conditioned media. 4) In situ hybridization of tPA and PAI-I mRNAs in the cultured granulosa cells also showed that PRL was capable of enhancing PAI-I mRNA while diminishing tPA mRNA production induced by LH. This suggests that the dose- and time-dependent decrease in the gonadotropin-induced tPA activity in the culture by the presence of PRL may be due to decreasing tPA mRNA synthesis on one hand and to neutralization of the tPA activity by the increased PAI-I activity on the other.
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| 4. |
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| 5. |
- Herrera-Marschitz, M, et al.
(författare)
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On the origin of extracellular glutamate levels monitored in the basal ganglia of the rat by in vivo microdialysis
- 1996
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Ingår i: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 66:4, s. 1726-1735
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Tidskriftsartikel (refereegranskat)abstract
- Several putative neurotransmitters and metabolites were monitored simultaneously in the extracellular space of neostriatum, substantia nigra, and cortex and in subcutaneous tissue of the rat by in vivo microdialysis. Glutamate (Glu) and aspartate (Asp) were at submicromolar and gamma-aminobutyric acid (GABA) was at nanomolar concentrations in all brain regions. The highest concentration of dopamine (DA) was in the neostriatum. Dynorphin B (Dyn B) was in the picomolar range in all brain regions. Although no GABA, DA, or Dyn B could be detected in subcutaneous tissue, Glu and Asp levels were 5 and approximately 5 and approximately 0.4 microM, respectively. Lactate and pyruvate concentrations were approximately 200 and approximately 10 microM in all regions. The following criteria were applied to ascertain the neuronal origin of substances quantified by microdialysis: sensitivity to (a) K+ depolarization, (b) Na+ channel blockade, (c) removal of extracellular Ca2+, and (d) depletion of presynaptic vesicles by local administration of alpha-latrotoxin. DA, Dyn B, and GABA largely satisfied all these criteria. In contrast, Glu and Asp levels were not greatly affected by K+ depolarization and were increased by perfusing with tetrodotoxin or with Ca2+-free medium, arguing against a neuronal origin. However, Glu and Asp, as well as DA and GABA, levels were decreased under both basal and K+-depolarizing conditions by alpha-latrotoxin. Because the effect of K+ depolarization on Glu and Asp could be masked by reuptake into nerve terminals and glial cells, the reuptake blocker dihydrokainic acid (DHKA) or L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) was included in the microdialysis perfusion medium. The effect of K+ depolarization on Glu and Asp levels was increased by DHKA, but GABA levels were also affected. In contrast, PDC increased only Glu levels. It is concluded that there is pool of releasable Glu and Asp in the rat brain. However, extracellular levels of amino acids monitored by in vivo microdialysis reflect the balance between neuronal release and reuptake into surrounding nerve terminals and glial elements.
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| 6. |
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| 7. |
- Weston, M. D., et al.
(författare)
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Myosin VIIA mutation screening in 189 Usher syndrome type 1 patients
- 1996
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Ingår i: American Journal of Human Genetics. - 0002-9297 .- 1537-6605. ; 59:5, s. 1074-1083
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Tidskriftsartikel (refereegranskat)abstract
- Usher syndrome type 1b (USH1B) is an autosomal recessive disorder characterized by congenital profound hearing loss, vestibular abnormalities, and retinitis pigmentosa. The disorder has recently been shown to be caused by mutations in the myosin VIIa gene (MYO7A) located on 11q14. In the current study, a panel of 189 genetically independent Usher I cases were screened for the presence of mutations in the N-terminal coding portion of the motor domain of MYO7A by heteroduplex analysis of 14 exons. Twenty-three mutations were found segregating with the disease in 20 families. Of the 23 mutations, 13 were unique, and 2 of the 13 unique mutations (Arg212His and Arg212Cys) accounted for the greatest percentage of observed mutant alleles (8/23, 31%). Six of the 13 mutations caused premature stop codons, 6 caused changes in the amino acid sequence of the myosin VIIa protein, and 1 resulted in a splicing defect. Three patients were homozygotes or compound heterozygotes for mutant alleles; these three cases were Tyr333Stop/Tyr333Stop, Arg212His-Arg302His/Arg212His-Arg302His, and IVS13nt-8c-->g/Glu450Gln. All the other USH1B mutations observed were simple heterozygotes, and it is presumed that the mutation on the other allele is present in the unscreened regions of the gene. None of the mutations reported here were observed in 96 unrelated control samples, although several polymorphisms were detected. These results add three patients to single case reported previously where mutations have been found in both alleles and raises the total number of unique mutations in MYO7A to 16.
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