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先天性骨质石化突变作为破骨细胞起源、结构和功能的研究探针。

Congenital osteopetrotic mutations as probes of the origin, structure, and function of osteoclasts.

作者信息

Marks S C

出版信息

Clin Orthop Relat Res. 1984 Oct(189):239-63.

PMID:6434217
Abstract

Progress has been made in recent years on the cell biology of the osteoclast and the pathogenesis of congenital osteopetrosis. New information is critically evaluated and summarized with respect to the origin, structure, and function of osteoclasts with special reference to osteopetroses. A broader perspective emerges from which to consider the biology of osteoclasts, the heterogeneities in the osteopetroses, and the value of each in elucidating the other, along with treatment of the disorder.

摘要

近年来,破骨细胞的细胞生物学及先天性骨硬化症的发病机制研究取得了进展。本文对有关破骨细胞的起源、结构和功能的新信息进行了批判性评估和总结,特别提及了骨硬化症。由此形成了一个更广阔的视角,用以思考破骨细胞生物学、骨硬化症的异质性、二者在阐释对方过程中的价值以及该疾病的治疗方法。

相似文献

1
Congenital osteopetrotic mutations as probes of the origin, structure, and function of osteoclasts.先天性骨质石化突变作为破骨细胞起源、结构和功能的研究探针。
Clin Orthop Relat Res. 1984 Oct(189):239-63.
2
Osteoclast biology: lessons from mammalian mutations.破骨细胞生物学:来自哺乳动物突变的启示。
Am J Med Genet. 1989 Sep;34(1):43-54. doi: 10.1002/ajmg.1320340110.
3
Experimental studies of osteopetrosis in laboratory animals.实验动物骨硬化症的实验研究。
Clin Orthop Relat Res. 1993 Sep(294):23-33.
4
The hematogenous origin of osteoclasts: experimental evidence from osteopetrotic (microphthalmic) mice treated with spleen cells from beige mouse donors.
Am J Anat. 1981 May;161(1):1-10. doi: 10.1002/aja.1001610102.
5
Coexistence of reduced function of natural killer cells and osteoclasts in two distinct osteopetrotic mutations in the rat.
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6
Evidence for a relationship between lymphoid cells and osteoclasts: bone resorption restored in ia (osteopetrotic) rats by lymphocytes, monocytes and macrophages from a normal littermate.
Am J Anat. 1978 Jul;152(3):331-41. doi: 10.1002/aja.1001520306.
7
Osteopetrosis in mice lacking haematopoietic transcription factor PU.1.缺乏造血转录因子PU.1的小鼠中的骨质石化症
Nature. 1997 Mar 6;386(6620):81-4. doi: 10.1038/386081a0.
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Osteoclast biology in the osteopetrotic (op) rat.骨石化(op)大鼠中的破骨细胞生物学
Am J Anat. 1989 Dec;186(4):325-34. doi: 10.1002/aja.1001860402.
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The origin of osteoclasts.破骨细胞的起源。
Immunobiology. 1982 Apr;161(3-4):193-203. doi: 10.1016/S0171-2985(82)80074-0.
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Human osteopetrosis and other sclerosing disorders: recent genetic developments.人类骨硬化症及其他硬化性疾病:近期遗传学进展
Calcif Tissue Int. 2001 Jul;69(1):1-6. doi: 10.1007/s002230020046. Epub 2001 Jun 5.

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Src is required for migration, phagocytosis, and interferon beta production in Toll-like receptor-engaged macrophages.Src是Toll样受体激活的巨噬细胞迁移、吞噬作用和干扰素β产生所必需的。
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New knowledge on critical osteoclast formation and activation pathways from study of rare genetic diseases of osteoclasts: focus on the RANK/RANKL axis.
从破骨细胞罕见遗传性疾病的研究中获得的关于破骨细胞形成和激活途径的新知识:关注 RANK/RANKL 轴。
Osteoporos Int. 2011 Jan;22(1):1-20. doi: 10.1007/s00198-010-1272-8. Epub 2010 May 11.
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A defect in inducible beta-galactosidase of B lymphocytes in the osteopetrotic (mi/mi) mouse.骨石化(mi/mi)小鼠B淋巴细胞中诱导型β-半乳糖苷酶的缺陷。
Immunology. 1996 Aug;88(4):604-10. doi: 10.1046/j.1365-2567.1996.d01-684.x.
5
Failure of calcitriol treatment in a patient with malignant osteopetrosis.
Eur J Pediatr. 1993 Oct;152(10):818-21. doi: 10.1007/BF02073378.
6
Malignant osteopetrosis: c-src kinase is not reduced in fibroblasts.恶性骨硬化症:成纤维细胞中的c-src激酶未减少。
Calcif Tissue Int. 1993 Jul;53(1):69-70. doi: 10.1007/BF01352018.
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The regulation of hemopoiesis in the spleen.脾脏中造血作用的调节。
Experientia. 1985 Feb 15;41(2):192-9. doi: 10.1007/BF02002613.
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Survival and resorptive activity of chick osteoclasts in culture.培养的鸡破骨细胞的存活及吸收活性
Anat Embryol (Berl). 1986;174(2):265-75. doi: 10.1007/BF00824342.
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Osteoclast generation from human fetal bone marrow in cocultures with murine fetal long bones. A model for in vitro study of human osteoclast formation and function.人胎儿骨髓与鼠胎儿长骨共培养体系中破骨细胞的生成。一种用于体外研究人破骨细胞形成及功能的模型。
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Cellular response to ectopically implanted silk sutures and osteopetrotic bone.细胞对异位植入的丝线缝合线和骨硬化骨的反应。
Cell Tissue Res. 1987 Apr;248(1):79-88. doi: 10.1007/BF01239966.