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Marked reduction of spectrinin hereditary spherocytosis in the common house mouse.

作者信息

Greenquist A C, Shohet S B, Bernstein S E

出版信息

Blood. 1978 Jun;51(6):1149-55.

PMID:647119
Abstract

In contrast to the disease in humans, hereditary spherocytosis in the common house mouse produces an extreme spherocytosis. The cells show a broad distribution in size ranging from microcytic to macrocytic. Of particular interest is the finding of a substantial reduction in the major membrane polypeptide called spectrin, supporting a critical role for this protein in the control of erythrocyte shape and membrane stability.

摘要

相似文献

1
Marked reduction of spectrinin hereditary spherocytosis in the common house mouse.
Blood. 1978 Jun;51(6):1149-55.
2
Deficient red-cell spectrin in severe, recessively inherited spherocytosis.严重隐性遗传性球形红细胞增多症中红细胞血影蛋白缺乏
N Engl J Med. 1982 May 13;306(19):1155-61. doi: 10.1056/NEJM198205133061906.
3
Spectrin and spherocytosis.血影蛋白与球形红细胞症
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Red cell membrane protein abnormalities in hereditary spherocytosis in Brazil.巴西遗传性球形红细胞增多症中的红细胞膜蛋白异常
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[Application of 2 electrophoresis techniques to the analysis of erythrocyte membrane proteins in hereditary spherocytosis].[两种电泳技术在遗传性球形红细胞增多症红细胞膜蛋白分析中的应用]
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Reductions of erythrocyte membrane viscoelastic coefficients reflect spectrin deficiencies in hereditary spherocytosis.红细胞膜粘弹性系数的降低反映了遗传性球形红细胞增多症中的血影蛋白缺陷。
J Clin Invest. 1988 Jan;81(1):133-41. doi: 10.1172/JCI113284.
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Lipid loss in spectrin deficient mouse erythrocytes.血影蛋白缺陷型小鼠红细胞中的脂质损失。
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Partial ankyrin and spectrin deficiency in severe, atypical hereditary spherocytosis.严重非典型遗传性球形红细胞增多症中的部分锚蛋白和血影蛋白缺乏
N Engl J Med. 1988 Jan 28;318(4):230-4. doi: 10.1056/NEJM198801283180407.
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[Hereditary spherocytosis: one year study of erythrocyte membrane proteins].[遗传性球形红细胞增多症:红细胞膜蛋白的一年研究]
Rev Med Brux. 1998 Oct;19(5 Pt 1):417-23.
10
A neonate with Coombs-negative hemolytic jaundice with spherocytes but normal erythrocyte indices: a rare case of autosomal-recessive hereditary spherocytosis due to alpha-spectrin deficiency.一名新生儿出现 Coombs 阴性溶血性黄疸伴球形红细胞但红细胞指数正常:一种罕见的常染色体隐性遗传性球形红细胞增多症,由α- spectrin 缺乏引起。
J Perinatol. 2013 May;33(5):404-6. doi: 10.1038/jp.2012.67.

引用本文的文献

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Regulation of Actin Dynamics in the Somatic Gonad.体细胞性腺中肌动蛋白动力学的调控
J Dev Biol. 2019 Mar 20;7(1):6. doi: 10.3390/jdb7010006.
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Spectrin regulates cell contractility through production and maintenance of actin bundles in the Caenorhabditis elegans spermatheca. spectrin 通过在秀丽隐杆线虫受精囊中原生肌动蛋白束的产生和维持来调节细胞收缩性。
Mol Biol Cell. 2018 Oct 1;29(20):2433-2449. doi: 10.1091/mbc.E18-06-0347. Epub 2018 Aug 9.
3
β-III spectrin is critical for development of purkinje cell dendritic tree and spine morphogenesis.
β-III spectrin 对于浦肯野细胞树突和棘突形态发生的发育至关重要。
J Neurosci. 2011 Nov 16;31(46):16581-90. doi: 10.1523/JNEUROSCI.3332-11.2011.
4
Analysis of the red cell membrane in a family with hereditary elliptocytosis--total or partial of protein 4.1.对一个遗传性椭圆形红细胞增多症家族的红细胞膜进行分析——蛋白质4.1完全或部分缺失。
Hum Genet. 1981;59(1):68-71. doi: 10.1007/BF00278857.
5
Of mice and men: the mice were right.《人鼠之间》:老鼠是对的。
J Clin Invest. 1995 Mar;95(3):921-2. doi: 10.1172/JCI117797.
6
Lateral diffusion in biological membranes. A normal-mode analysis of diffusion on a spherical surface.生物膜中的横向扩散。球面上扩散的简正模式分析。
Biophys J. 1980 Apr;30(1):187-92. doi: 10.1016/S0006-3495(80)85087-9.
7
Matrix control of protein diffusion in biological membranes.生物膜中蛋白质扩散的基质控制
Proc Natl Acad Sci U S A. 1981 Jun;78(6):3576-80. doi: 10.1073/pnas.78.6.3576.
8
Elliptical erythrocyte membrane skeletons and heat-sensitive spectrin in hereditary elliptocytosis.遗传性椭圆形红细胞增多症中的椭圆形红细胞膜骨架和热敏感血影蛋白
Proc Natl Acad Sci U S A. 1981 Mar;78(3):1911-5. doi: 10.1073/pnas.78.3.1911.
9
Deficiency of skeletal membrane protein band 4.1 in homozygous hereditary elliptocytosis. Implications for erythrocyte membrane stability.纯合子遗传性椭圆形红细胞增多症中骨骼膜蛋白带4.1的缺乏。对红细胞膜稳定性的影响。
J Clin Invest. 1981 Aug;68(2):454-60. doi: 10.1172/jci110275.
10
Electron microscopic study of reassociation of spectrin and actin with the human erythrocyte membrane.血影蛋白和肌动蛋白与人红细胞膜重新结合的电子显微镜研究。
J Cell Biol. 1981 Jul;90(1):70-7. doi: 10.1083/jcb.90.1.70.