https://www.selleckchem.com/pr....oducts/ezatiostat.ht
We found that all pathological mutations examined reduce atlastin activity in vivo although to different degrees of severity. Moreover, overexpression of the pathogenic variants in a wild type atlastin background does not give rise to the loss of function phenotypes expected for dominant negative mutations. These results indicate that the four pathological mutations investigated act through a loss of function mechanism. To investigate the role of CAB39 in nasopharyngeal carcinoma (NPC) development and examine its expression level in
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