EC Number |
General Information |
Reference |
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3.5.4.37 | malfunction |
A-to-I underediting at the glutamine (Q)/arginine (R) site of the glutamate receptor subunit B (GluR-B) is associated with the pathogenesis and invasiveness of glioma and is confirmed in the glioma cell lines U87, U251 and A172 compared with that in normal human astrocytes. The expression of ADAR2 mRNA was not significantly altered in the glioma cell lines. Aberrant alternative splicing pattern of ADAR2 downregulates A-to-I editing in glioma |
757880 |
3.5.4.37 | malfunction |
ADAR1 knockout embryos die at day 11.5 to 12. ADAR1 is not completely necessary for cell survival because some cells survive without ADAR1. ADAR1 is dispensable in pluripotent cells for their survival and proliferation |
718816 |
3.5.4.37 | malfunction |
ADAR1-/- homozygous embryos die at E11.0 to E12.5. Widespread apoptosis is detected in many tissues of ADAR1-/- embryos collected live at E10.5 to E11.5, despite their normal gross appearance |
719826 |
3.5.4.37 | malfunction |
dysregulation of A-to-I editing by ADAR1 can have profound consequences, ranging from effects on cell growth and development to autoimmune disorders |
757223 |
3.5.4.37 | malfunction |
homozygosity for two different null alleles of ADAR1 causes a consistent embryonic phenotype appearing early at embryonic day 11 and leading to death between embryonic days 11.5 and 12.5. This phenotype manifests a rapidly disintegrating liver structure, along with severe defects in definitive hematopoiesis, encompassing both erythroid and myeloid/granuloid progenitors as well as spleen colonyforming activity from the aorta-gonad-mesonephros region and fetal liver |
719824 |
3.5.4.37 | malfunction |
interferon treatment of Adar1-/-x02cells lacking both the p110 constitutive and p150 interferon-inducible ADAR1 proteins induces formation of stress granules, whereas neither wild-type nor Adar2x02-/-x02 cells display a comparable stress granule response following interferon treatment. Phosphorylation of protein synthesis initiation factor eIF2alpha at Ser51 is increased in interferon-treated Adar1x02-/-x02cells but not in either wild-type or Adar2x02-/- cells following interferon treatment |
757170 |
3.5.4.37 | malfunction |
knock-down of ADAR1 increases HIV-1 replication in primary macrophages |
735124 |
3.5.4.37 | malfunction |
knockdown of ADAR by RNA interference induces formation of pseudo-diapause embryos, which lack resistance to the stresses and exhibit high levels of apoptosis |
758478 |
3.5.4.37 | malfunction |
knockdown of ADAR2 expression markedly impairs glucose-stimulated insulin secretion in the rat insulinoma INS-1 cells and primary pancreatic islets and significantly diminishes KCl-stimulated secretion of exogenous human growth hormone or endogenous chromogranin B protein in the rat adrenal pheochromocytoma PC12 cells |
719435 |
3.5.4.37 | malfunction |
knockdown of ADARa in lung adenocarcinoma cells with amplified ADAR leads to decreased migration and invasion |
758458 |