REGULATION OF PARATHYROID FUNCTION
REGULATION OF PARATHYROID FUNCTION
批准号:
3229325
负责人:
JEREMIAH J MORRISSEY
金额:
$10.25万
依托单位国家:
美国
项目类别:
财政年份:
1991
资助国家:
美国
项目状态:
已结题
起止时间:
1991-09-01 至 1993-06-30
关键词:
G protein adenosine diphosphate adenylate cyclase biological signal transduction calcium binding protein calcium channel calcium metabolism cell membrane cyclic AMP cytoskeletal proteins epitope mapping glycosylation hormone regulation /control mechanism lipid metabolism membrane lipids membrane permeability myristates parathyroid gland pertussis toxin phorbols phosphatidylinositols phospholipase A2 phosphorylation protein kinase C protein metabolism secretion western blottings
中文摘要
描述(改编自申请人的摘要):主要
甲状旁腺机能亢进症是一种相对常见的内分泌功能障碍,伴有
发病率为每10万人口40-45例。次要的
甲状旁腺机能亢进是肾功能衰竭的一种表现。已经结束了
美国有10万名接受透析的患者。因此,失调症
甲状旁腺功能给医疗保健管理带来巨大负担
以及每年的劳动力流失。甲状旁腺的控制
激素分泌几乎是独一无二的,因为钙最终会抑制
分泌,而在大多数其他系统中,钙刺激分泌。这
研究的重点是涉及到的分子机制。
控制钙介导的甲状旁腺素分泌。GTP结合信号的作用
正常甲状旁腺分泌物中的转导蛋白和蛋白激酶C
将会被研究。将使用合成的寡核苷酸探针来选择
正常牛甲状旁腺表达文库中的DNA序列
构建于噬菌体lambda gtl0中。与该信号相对应的DNA
转导蛋白将通过双脱氧基进行亚克隆和测序
链终止法推断GTP结合蛋白的类型
在甲状旁腺细胞中表达。这将确定是否
甲状旁腺细胞含有其他细胞共有的信号转导蛋白
分泌组织,或者如果有一种独特的转导蛋白
甲状旁腺激素,可解释钙敏感性的逆转
荷尔蒙分泌。根据衍生的氨基酸序列、多肽
将合成特定序列的。这些多肽将被用于
产生针对单个信号转导的多克隆抗血清
蛋白质,以便在甲状旁腺细胞中对这些蛋白质进行定量。这个
作为百日咳毒素和百日咳毒素底物的转导蛋白
霍乱毒素和一种与磷脂酶C连锁的毒素不敏感蛋白
将被描述为。百日咳毒素和霍乱毒素对小鼠免疫功能的影响
钙、镁和锶对甲状旁腺激素分泌的抑制作用
细胞内钙离子的变化将被评估。蛋白激酶的作用
甲状旁腺分泌物中的C将通过监测酶活性来评估,
并通过使用针对三种抗体的抗肽抗血清
蛋白激酶C.Sphingoid碱基代谢的异构体
细胞外钙、镁和锶将被评估为
蛋白激酶C抑制剂的生产。这些研究利用了
甲状旁腺表达文库、DNA测序及抗肽抗体
将构成今后检查正常和异常的基础
甲状旁腺功能。
英文摘要
DESCRIPTION (Adapted from the Applicant's Abstract): Primary
hyperparathyroidism is a relatively common endocrine dysfunction with an
incidence of 40-45 cases per 100,000 population. Secondary
hyperparathyroidism is a manifestation of renal failure. There are over
100,000 patients on dialysis in the United States. Thus, disorders of
parathyroid function impose a significant burden on health care management
and loss from the labor force each year. The control of parathyroid
hormone secretion is almost unique in that calcium ultimately inhibits
secretion whereas in most other systems calcium stimulates secretion. This
investigation focuses on molecular mechanisms that are involved in the
control of calcium-mediated PTH secretion. The role of GTP-binding signal
transducing proteins and protein kinase C in normal parathyroid secretion
will be studied. Synthetic oligonucleotide probes will be used to select
for DNA sequences in a normal bovine parathyroid expression library
constructed in phage lambda gtl0. The DNA corresponding to the signal
transduction proteins will be subcloned and sequenced by the dideoxy
chain-termination method to deduce the types of GTP-binding proteins
expressed in the parathyroid cell. This will establish whether the
parathyroid cell contains signal transduction proteins common to other
secretory tissues, or if there is a unique transducing protein to the
parathyroid which can account for the reverse calcium sensitivity of
hormone secretion. Based upon the derived amino acid sequences, peptides
of specific sequence will be synthesized. These peptides will be used to
generate polyclonal antisera specific to the individual signal transduction
proteins in order to quantitate these proteins in parathyroid cells. The
transducing proteins which serve as substrates for pertussis toxin and
cholera toxin, and a toxin-insensitive protein linked to phospholipase C
will be characterized. The effect of pertussis toxin and cholera toxin on
calcium, magnesium and strontium-induced suppression of PTH secretion and
changes in cytosolic calcium will be evaluated. The role of protein kinase
C in parathyroid secretion will be evaluated by monitoring enzyme activity,
and through the use of anti-peptide antisera specific for the three
isoforms of protein kinase C. Sphingoid base metabolism as a function of
extracellular calcium, magnesium and strontium will be evaluated for the
production of protein kinase C inhibitors. These studies utilizing the
parathyroid expression library, DNA sequencing and antipeptide antibodies
will form a basis for the future examination of normal and abnormal
parathyroid function.
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Effect of 1,25-dihydroxyvitamin D3 on phospholipid metabolism in cultured bovine parathyroid cells.
1,25-二羟基维生素 D3 对培养牛甲状旁腺细胞磷脂代谢的影响。
DOI:
10.1210/endo-122-6-2387
发表时间:
1988
期刊:
Endocrinology
影响因子:
4.8
作者:
[Sugimoto,T, Ritter,C, Slatopolsky,E, Morrissey,J]
通讯作者:
Morrissey,J
A new analog of 1,25-(OH)2D3, 19-NOR-1,25-(OH)2D2, suppresses serum PTH and parathyroid gland growth in uremic rats without elevation of intestinal vitamin D receptor content.
1,25-(OH)2D3 的新类似物 19-NOR-1,25-(OH)2D2 可抑制尿毒症大鼠的血清 PTH 和甲状旁腺生长,而不升高肠道维生素 D 受体含量。
DOI:
10.1016/s0272-6386(97)90571-0
发表时间:
1997
期刊:
American journal of kidney diseases : the official journal of the National Kidney Foundation
影响因子:
--
作者:
[Takahashi,F, Finch,JL, Denda,M, Dusso,AS, Brown,AJ, Slatopolsky,E]
通讯作者:
Slatopolsky,E
DOI:
10.1038/ki.2011.23
发表时间:
2011-04
期刊:
Kidney international. Supplement
影响因子:
--
作者:
[]
通讯作者:
1,25-Dihydroxy-19-nor-vitamin D(2), a vitamin D analog with reduced bone resorbing activity in vitro.
1,25-二羟基-19-去甲维生素 D(2),一种维生素 D 类似物,在体外具有降低骨吸收活性。
DOI:
10.1681/asn.v11101857
发表时间:
2000
期刊:
Journal of the American Society of Nephrology : JASN
影响因子:
--
作者:
[Holliday,LShannon, Gluck,StephenL, Slatopolsky,Eduardo, Brown,AlexJ]
通讯作者:
Brown,AlexJ
Suppression of PTH and decreased action on bone are partially responsible for the low calcemic activity of 22-oxacalcitriol relative to 1,25-(OH)2D3.
PTH 的抑制和对骨作用的降低是 22-奥沙骨化三醇相对于 1,25-(OH)2D3 的低钙血活性的部分原因。
DOI:
10.1002/jbmr.5650070713
发表时间:
1992
期刊:
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
影响因子:
--
作者:
[Finch,JL, Brown,AJ, Mori,T, Nishii,Y, Slatopolsky,E]
通讯作者:
Slatopolsky,E
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