ATM is versatile member of DNA damage repair mechanism, involved in monitoring the genomic integrity. Any damage done to DNA relentlessly challenges this guardian’s credibility. This multitalented mediator comes into action to recapitulate faithfully the derailed genomics. Double stranded breaks are a consistent threat and actively implicated in tipping the scales of cancer in favor of genomic instability. Therefore it holds great potential in safeguarding and resolving efficiently abrupt aberrations. According to the increasing sophisticated information, ATM silencing and stimulation, both are being evaluated for a better therapeutic intervention. In this review we will analyze both paradigms of rational drug design. Taking into consideration, the emerging snapshot of push and pull between diametrically opposed roles of ATM, there is an urgent requirement to tailor therapies with promising clinical outcomes.
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