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ÇëÎÊ off-target ׼ȷ·­ÒëΪɶ£¿ÎÒ˵ÊÇÍѰУ¬Ð¡Àϰå˵²»¶ÔÓ¦¸ÃÊÇÔ¶¸ô¡£¡£¡£ËùÒÔ¾¿¾¹ÊÇɶÒâ˼£¿

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max_dolphin(ANDPing´ú·¢): ½ð±Ò+2, ¸ÐлӦÖú£¬»¶Ó­³£À´×¨ÒµÍâÓï°æ½»Á÷ѧϰ 2018-12-16 13:09:48
max_dolphin(¿Õλ´ú·¢): ½ð±Ò+1, ¸Ðл½»Á÷ 2018-12-25 21:21:37
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max_dolphin(¿Õλ´ú·¢): ½ð±Ò+2, ¸Ðл½»Á÷ 2018-12-25 21:21:18
Off-target activity is biological activity of a drug that is different from and not at that of its intended biological target. It most commonly contributes to side effects. However, in some cases, off-target activity can be taken advantage of for therapeutic purposes. An example of this is the repurposing of the antimineralocorticoid and diuretic spironolactone, which was known to produce feminization and gynecomastia as side effects, for use as an antiandrogen in the treatment of conditions like acne and hirsutism.

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Off-target genome editing refers to nonspecific and unintended genetic modifications that can arise through the use of engineered nuclease technologies such as: clustered, regularly interspaced, short palindromic repeats (CRISPR)-Cas9, transcription activator-like effector nucleases (TALEN), meganucleases, and zinc finger nucleases (ZFN).[1] These tools use different mechanisms to bind a predetermined sequence of DNA (¡°target¡±), which they cleave (or "cut", creating a double-stranded chromosomal break (DSB) that summons the cells DNA repair mechanisms (non-homologous end joining (NHEJ) and homologous recombination (HR)) and leads to site-specific modifications.[2] If these complexes do not bind at the target, often a result of homologous sequences and/or mismatch tolerance, they will cleave off-target DSB and cause non-specific genetic modifications.[3][4][5] Specifically, off-target effects consist of unintended point mutations,[6] deletions,[7][8] insertions[5] inversions,[5] and translocations.[9][8]
3Â¥2018-08-28 23:26:50
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