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• Journal article
  MacCabe AP, vandenHombergh JPTW, Tilburn J, Arst HN, Visser Jet al., 1996,

  Identification, cloning and analysis of the Aspergillus niger gene pacC, a wide domain regulatory gene responsive to ambient pH

  , MOLECULAR AND GENERAL GENETICS, Vol: 250, Pages: 367-374, ISSN: 0026-8925
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  • Citations: 55
• Journal article
  Byrne B, Fowler PA, Templeton AA, 1996,

  The effects of steroidal and non-steroidal ovarian factors on the pituitary responsiveness to gonadotrophin surge attenuating factor.

  , Journal of Endocrinology, Vol: 150, Pages: 413-422

  Primary pituitary cultures from adult female rats were used to investigate the effects of steroidal (oestradiol and progesterone) and non-steroidal (inhibin, follistatin) ovarian hormones on the suppressive actions of the ovarian factor gonadotrophin surge-attenuating factor (GnSAF) in the control of gonadotrophin secretion. The source of GnSAF was a chromatographic preparation from follicular fluid containing four distinct protein bands as resolved on SDS-PAGE. Oestradiol and progesterone added alone had no effect on gonadotrophin secretion but had a wide range of effects on the suppression of both LH and FSH secretion caused by the non-steroidal factors. Oestradiol, progesterone and oestradiol+progesterone enhanced the suppressive actions of GnSAF on GnRH-induced LH secretion (causing 19.3 +/- 5.2% (P < 0.05), 41.9 +/- 3.4% (P < 0.001) and 32.2 +/- 5.3% (P < 0.001) greater suppression than GnSAF alone). Progesterone and oestradiol+progesterone completely abolished the suppression of basal FSH secretion caused by inhibin (causing 157.1 +/- 22.2%, P < 0.001, and 160.9 +/- 11.3%, P < 0.001, stimulation compared with inhibin alone). Separately the steroids had no effect on the suppression of gonadotrophin secretion caused by follistatin. However, in combination, oestradiol+progesterone potentiated the suppressive actions of follistatin on GnRH-induced LH secretion causing 29.9 +/- 5.3% (P < 0.05) greater suppression than follistatin alone. In combination, high-dose follistatin and GnSAF caused 31.1 +/- 6.5% (P < 0.01) greater suppression than GnSAF alone. Thus in combination high-dose follistatin and GnSAF have additive effects on the suppression of GnRH-induced LH secretion. Recombinant human inhibin and GnSAF added in combination had little further effect compared with either alone suggesting that they may have a similar mechanism of action at the pituitary level. These results demonstrate that while FSH secretion in vitro is mainly controlled b

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• Journal article
  Byrne B, Fowler PA, Templeton AA, 1996,

  Gonadotrophin surge attenuating factor suppresses progesterone augmentation of GnRH priming

  , Journal of Clinical Endocrinology & Metabolism, Vol: 81, Pages: 1454-1459

  We investigated the effects of gonadotropin surge-attenuating factor (GnSAF), inhibin, and follistatin on GnRH self-priming and its augmentation by progesterone. Two GnRH challenges, 60 min apart, were administered to rat pituitary monolayers after 90-min exposure to medium alone (control), progesterone, GnSAF, inhibin, or follistatin. Inhibin-stripped follicular fluid from superovulated women was used as a source of GnSAF bioactivity. Under control conditions, the greater response to the second GnRH challenge (peak 2, 9.2 +/- 2.1; peak 1, 4.4 +/- 0.9 ng LH/mL; P < 0.01) demonstrated GnRH self-priming. None of the treatments significantly altered the first LH peak. Progesterone markedly increased GnRH self-priming (peak 2, 12.6 +/- 2.5 ng LH/mL; P < 0.01). However, GnSAF and RU486 significantly reduced GnRH self-priming (peak 2, 4.6 +/- 0.9 and 5.6 +/- 1.6 ng LH/mL, respectively; P < 0.01). The augmentation of self-priming induced by progesterone was completely abolished by coincubation with either GnSAF or RU486 (peak 2, 7.5 +/- 1.6 and 4.3 +/- 0.9 ng LH/mL, respectively; P < 0.01). Neither inhibin nor follistatin had any effect on GnRH self-priming or its augmentation by progesterone. The actions of RU486 in the presence and absence of progesterone demonstrate a nonprogestagenic effect of RU486 on the gonadotropes. In conclusion, the suppression of GnRH self-priming, with or without progesterone augmentation, supports the hypothesis that GnSAF acts by maintaining the pituitary in an unprimed state of reduced responsiveness to GnRH.

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• Journal article
  Platt A, Langdon T, Arst HN, Kirk D, Tollervey D, Mates Sanchez JM, Caddick MXet al., 1996,

  Nitrogen metabolite signalling involves the C-terminus and the GATA domain of the Aspergillus transcription factor AREA and the 3' untranslated region of its mRNA

  , EMBO J, Vol: 15, Pages: 2791-2801
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• Journal article
  Moffatt MF, Cookson WO, 1996,

  The genetics of specific allergy.

  , Monogr Allergy, Vol: 33, Pages: 71-96, ISSN: 0077-0760
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• Journal article
  Platt A, Ravagnani A, Arst H, Kirk D, Langdon T, Caddick Met al., 1996,

  Mutational analysis of the C-terminal region of AREA, the transcription factor mediating nitrogen metabolite repression in Aspergillus nidulans

  , Molecular Gen Genet, Vol: 250, Pages: 106-114
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• Conference paper
  Cookson W, 1996,

  Genetic factors in asthma.

  , Pages: 55-60, ISSN: 0065-2598
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• Book chapter
  Arst HN, Sheerins A, 1996,

  Regulation of gene expression by pH

  , The Mycota, Editors: Brambl, Marzluf, Berlin, Publisher: Springer-Verlag, Pages: 235-240
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• Journal article
  DENISON SH, OREJAS M, ARST HN, 1995,

  SIGNALING OF AMBIENT PH IN ASPERGILLUS INVOLVES A CYSTEINE PROTEASE

  , JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 270, Pages: 28519-28522, ISSN: 0021-9258
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  • Citations: 123
• Conference paper
  Cookson WO, 1995,

  11q and high-affinity IgE receptor in asthma and allergy.

  , Pages: 71-73, ISSN: 0954-7894
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