Analyzing the mechanism of RS formation

NIAID Data Ecosystem2026-05-01 收录

环形铁粒幼细胞形成机制

SF3B1突变分子机制

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https://www.ncbi.nlm.nih.gov/sra/DRP008934 数据链接链接失效反馈

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In order to studyng the relationship of mutant SF3B1 and RS formation in myelodysplastic syndromes, RNA extracted from wild-type or mutant SF3B1 expressing erythroleukemic cell line (K562 cells) was analyzed.

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2023-08-10

Functional and conformational impact of cancer-associated SF3B1 mutations depends on the position and the charge of amino acid substitution

SF3B1突变分子机制

RNA-SEQ分析

RNA-sequencing data from HEK293T cell models: Hek293T transfected with expression vectors of SF3B1-WT, SF3B1-R625H, SF3B1-K666T, SF3B1-K700E. Overall design: In cellulo examination of SF3B1 mutations

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Selinexor, a First-in-Class XPO1 Inhibitor, Is Efficacious and Tolerable in Patients with Myelodysplastic Syndromes Refractory to Hypomethylating Agents. Selinexor, a First-in-Class XPO1 Inhibitor, Is Efficacious and Tolerable in Patients with Myelodysplastic Syndromes Refractory to Hypomethylating Agents

骨髓增生异常综合征

SF3B1突变分子机制

PURPOSE The median overall survival (OS) of patients with high-risk myelodysplastic syndromes (MDS) refractory to hypomethylating agents is less than 6 months and there is no standard therapy for such

NIAID Data Ecosystem10

Homo sapiens Raw sequence reads

RNA剪接分支点识别

SF3B1突变分子机制

SF3B1 is a component of U2, so we suspect that the SF3B1 K700E mutation may reduce the fidelity of branch site utilization. Lariats at loci with SF3B1 mutant alternate 3''ss usage are specifically tar

NIAID Data Ecosystem10

A genetic murine model of CLL based on B cell-restricted expression of Sf3b1 mutation and Atm deletion. A genetic murine model of CLL based on B cell-restricted expression of Sf3b1 mutation and Atm deletion

慢性淋巴细胞白血病(CLL)小鼠模型

SF3B1突变分子机制

The RNA splicing factor SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its functional role in the pathogenesis of this disease has not been firmly established. Here, we show t

NIAID Data Ecosystem20

SF3B1 mutant-induced missplicing of MAP3K7 causes anemia in myelodysplastic syndromes. SF3B1 mutant-induced missplicing of MAP3K7 causes anemia in myelodysplastic syndromes

骨髓增生异常综合征

SF3B1突变分子机制

SF3B1 is the most frequently mutated RNA splicing factor in cancer, including in ~25% of myelodysplastic syndromes (MDS) patients. SF3B1-mutated MDS, which is strongly associated with ringed siderobla

NIAID Data Ecosystem10

Analyzing the mechanism of RS formation

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