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Am J Hum Genet. 1998 May;62(5):1062-9. doi: 10.1086/301834.
2
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Codanin-1, the protein encoded by the gene mutated in congenital dyserythropoietic anemia type I (CDAN1), is cell cycle-regulated.科达宁-1(Codanin-1)是由I型先天性红细胞生成异常性贫血(CDAN1)中发生突变的基因所编码的蛋白质,其受细胞周期调控。
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本文引用的文献

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Exclusion of three candidate genes as determinants of congenital dyserythropoietic anemia type II (CDA-II).
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2
Localization of the congenital dyserythropoietic anemia II locus to chromosome 20q11.2 by genomewide search.通过全基因组搜索将先天性红细胞生成异常性贫血II型基因座定位于染色体20q11.2。
Am J Hum Genet. 1997 Nov;61(5):1112-6. doi: 10.1086/301609.
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Dyserythropoiesis and congenital dyserythropoietic anaemias.红细胞生成异常与先天性红细胞生成异常性贫血。
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Neonatal manifestations of congenital dyserythropoietic anemia type I.Ⅰ型先天性红细胞生成异常性贫血的新生儿表现
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Clinical features and studies of erythropoiesis in Israeli Bedouins with congenital dyserythropoietic anemia type I.以色列贝都因I型先天性红细胞生成异常性贫血患者的临床特征及红细胞生成研究
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Preferential localization of the limb-girdle muscular dystrophy type 2A gene in the proximal part of a 1-cM 15q15.1-q15.3 interval.2A型肢带型肌营养不良症基因在15q15.1 - q15.3区间1厘摩近端部分的优先定位。
Am J Hum Genet. 1995 Jun;56(6):1417-30.
8
Mutations in the proteolytic enzyme calpain 3 cause limb-girdle muscular dystrophy type 2A.蛋白水解酶钙蛋白酶3的突变会导致2A型肢带型肌营养不良症。
Cell. 1995 Apr 7;81(1):27-40. doi: 10.1016/0092-8674(95)90368-2.
9
Genetic analysis of idiopathic torsion dystonia in Ashkenazi Jews and their recent descent from a small founder population.德系犹太人特发性扭转性肌张力障碍的遗传分析及其近期源自一小群奠基者群体的情况。
Nat Genet. 1995 Feb;9(2):152-9. doi: 10.1038/ng0295-152.
10
Localization of the gene for congenital dyserythropoietic anemia type III, CDAN3, to chromosome 15q21-q25.先天性III型红细胞生成异常性贫血(CDAN3)基因定位于15号染色体q21-q25区域。
Hum Mol Genet. 1995 Jan;4(1):109-12. doi: 10.1093/hmg/4.1.109.

I型先天性红细胞生成异常性贫血基因定位于15号染色体15q15.1 - 15.3上小于1厘摩的区间。

Localization of the gene for congenital dyserythropoietic anemia type I to a <1-cM interval on chromosome 15q15.1-15.3.

作者信息

Tamary H, Shalmon L, Shalev H, Halil A, Dobrushin D, Ashkenazi N, Zoldan M, Resnitzky P, Korostishevsky M, Bonne-Tamir B, Zaizov R

机构信息

Pediatric Hematology Oncology Center, Schneider Children's Medical Center of Israel, Beilinson Campus, Petah Tiqva, Israel.

出版信息

Am J Hum Genet. 1998 May;62(5):1062-9. doi: 10.1086/301834.

DOI:10.1086/301834
PMID:9545404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1377091/
Abstract

Congenital dyserythropoietic anemias (CDA) are a rare group of red-blood-cell disorders of unknown etiology that are characterized by ineffective erythropoiesis, pathognomonic cytopathology of the nucleated red blood cells in the bone marrow, and secondary hemochromatosis. In CDA type I, bone-marrow electron microscopy reveals characteristic findings in erythroid precursors, including spongy heterochromatin and enlarged nuclear pores. Since the genetic basis of CDA type I is not evident, we used homozygosity and linkage mapping to localize the genetic defect responsible for CDA type I in 25 Bedouins from four large consanguineous families. We report the linkage of this disease to markers on chromosome 15 located at q15. 1-q15.3. Fourteen markers within a 12-cM interval were typed in the relevant family members. Nine of the markers yielded maximum LOD scores of 1.625-12.928 at a recombination fraction of .00. Linkage disequilibrium was found only with marker D15S779. Haplotype analysis revealed eight different carrier haplotypes and highlighted the existence of a founder haplotype. Identification of historical crossover events further narrowed the gene location to between D15S779 and D15S778. The data suggest localization of the CDA type I gene within a 0.5-cM interval. The founder mutation probably occurred >/= 400 years ago. Sequence analysis of the coding region of protein 4.2, the only known erythroid-specific gene in the locus, did not reveal any change in the CDA type I patients. Future analysis of this locus may lead to the identification of a gene essential to normal erythropoiesis.

摘要

先天性红细胞生成异常性贫血(CDA)是一组病因不明的罕见红细胞疾病,其特征为无效红细胞生成、骨髓中有核红细胞的特征性细胞病理学表现以及继发性血色素沉着症。在Ⅰ型CDA中,骨髓电子显微镜检查可发现红系前体细胞的特征性表现,包括海绵状异染色质和扩大的核孔。由于Ⅰ型CDA的遗传基础尚不明确,我们利用纯合性和连锁图谱分析,对来自四个大的近亲家族的25名贝都因人中导致Ⅰ型CDA的遗传缺陷进行定位。我们报告该疾病与位于15号染色体q15.1 - q15.3的标记连锁。在相关家庭成员中对一个12厘摩区间内的14个标记进行了分型。其中9个标记在重组率为0.00时产生的最大对数优势分数为1.625 - 12.928。仅发现与标记D15S779存在连锁不平衡。单倍型分析揭示了8种不同的携带者单倍型,并突出显示了一个始祖单倍型的存在。对历史交换事件的鉴定进一步将基因定位缩小到D15S779和D15S778之间。数据表明Ⅰ型CDA基因定位于一个0.5厘摩的区间内。始祖突变可能发生在≥400年前。对该位点唯一已知的红系特异性基因蛋白4.2编码区的序列分析未发现Ⅰ型CDA患者有任何变化。对该位点的进一步分析可能会鉴定出正常红细胞生成所必需的基因。