Human KRML (MAFB):: cDNA cloning, genomic structure, and evaluation as a candidate tumor suppressor gene in myeloid leukemias
Human KRML (MAFB):: cDNA cloning, genomic structure, and evaluation as a candidate tumor suppressor gene in myeloid leukemias
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DOI：
10.1006/geno.1999.5884
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发表时间：
1999-08-01
期刊：
影响因子：
4.4
通讯作者：
Le Beau, MM
中科院分区：
文献类型：
--
作者：
Wang, PW;Eisenbart, JD;Le Beau, MM
基本共振/亮氨酸拉链转录因子 MAF 家族的成员可以以正向或负向方式影响转录，具体取决于其伴侣蛋白和目标启动子的背景。 KRML (MAFB) 转录调节因子通过抑制骨髓细胞中 ETS1 介导的红系特异性基因转录，在调节谱系特异性造血过程中发挥关键作用。在之前的研究中，我们将人类 KRML 基因定位在人类 20 号染色体上的基因组重叠群中，带 q11.2-q13.1。我们已经分离出含有全长预测开放阅读框（ORF）的人类 cDNA。多个类似 1.8 和类似 3 kb 的 KRML 转录本，其 3' 非翻译区长度不同，在造血组织中普遍表达，并编码具有 323 个氨基酸（MW 35,832）的蛋白质。该蛋白与鼠蛋白有 84% 的同一性和 92% 的相似性。人类KRML基因的ORF不含内含子，基因跨度约为3 kb。 KRML 定位在以 20q 缺失为特征的恶性骨髓疾病中最小的常见缺失片段内；然而，我们在20q缺失的白血病细胞中没有检测到KRML突变，因此，KRML不太可能参与以20号染色体异常为特征的恶性骨髓疾病的发病机制。(C) 1999学术出版社。
Members of the MAF family of basic reson/leucine zipper transcription factors can affect transcription in either a positive or a negative fashion, depending on their partner protein(s) and the context of the target promoter. The KRML (MAFB) transcriptional regulator plays a pivotal role in regulating Lineage-specific hematopoiesis by repressing ETS1-mediated transcription of erythroid-specific genes in myeloid cells, In previous studies, we mapped the human KRML gene within a genomic contig on human chromosome 20, bands q11.2-q13.1. We have isolated the human cDNA containing the full-length predicted open reading frame (ORF). Multiple KRML transcripts of similar to 1.8 and similar to 3 kb, which differ in the length of the 3' untranslated region, are ubiquitously expressed in hematopoietic tissues and encode a protein with 323 amino acids (MW 35,832). The protein has 84% identity and 92% similarity to the murine protein. The ORF of the human KRML gene contains no introns, and the gene spans similar to 3 kb. KRML maps within the smallest commonly deleted segment in malignant myeloid disorders characterized by a deletion of 20q; however, we detected no mutations of KRML in leukemia cells with loss of 20q, Thus, KRML is unlikely to be involved in the pathogenesis of malignant myeloid disorders characterized by abnormalities of chromosome 20. (C) 1999 Academic Press.