EC Number |
General Information |
Reference |
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2.1.1.359 | malfunction |
ASH1 knockdown causes reduced expression of Hox genes. Knockdown of ASH1 in K-562 cells in vitro causes increased expression of epsilon-globin gene and reduced expression of myelomonocytic markers GPIIb and GPIIIa, whereas knockdown of ASH1 in haematopoietic stem cells in vivo results in decreased number of macrophages and granulocytes |
720843 |
2.1.1.359 | malfunction |
ashh2 mutants are defective in ovule and embryo sac development, mutation in ASHH2 leads to substantial changes in inflorescence gene expression |
706446 |
2.1.1.359 | malfunction |
cells lacking the enzyme display microsatellite instability and an elevated spontaneous mutation frequency, characteristic of DNA mismatch repair-deficient cells. Enzyme-deficient cells fail to recruit MutSalpha to chromatin |
753166 |
2.1.1.359 | malfunction |
enzyme downregulation leads to higher RNA polymerase II turnover at the transcription site and leads to intragenic transcription initiation in human cells |
754923 |
2.1.1.359 | malfunction |
enzyme knockdown affects processing of late viral RNAs |
755216 |
2.1.1.359 | malfunction |
enzyme knockdown in human endothelial cells impairs migration and tubule formation activities |
755239 |
2.1.1.359 | malfunction |
enzyme knockdown leads to defective repair of DNA double-strand breaks via the homologous recombination pathway |
754146 |
2.1.1.359 | malfunction |
enzyme knockdown significantly reduces survival after treatment with mitomycin C, camptothecin, or ionizing radiation in U2OS cells and HeLa cells |
753204 |
2.1.1.359 | malfunction |
enzyme loss is associated with alterations in mRNA splicing in human clear cell renal cell carcinoma |
754937 |
2.1.1.359 | malfunction |
enzyme mutants display pleiotropic defects, including typical brassinosteroid-deficient morphologies and late flowering associated with the down-regulation of the brassinosteroid pathway and flowering regulatory genes |
755045 |