Every time your cell divide , the “ telomeres , ” or caps on the remainder of your chromosomes , get a little short . senior creatures lead off to hurt diseases of sure-enough eld partly because their telomere have become so myopic , and cellular division becomes difficult and error - prone . That ’s why telomere are the subject of intensive study : If we could figure out the mechanism that keeps our telomeres from shortening , it ’s potential we could prolong our lives . Now a group of California researcher have discovered that a protein shout out Est3 ( pictured ) is partly responsible for keeping telomeres long . Manipulating that protein could bring us one step nearer to healthy cell longevity . As they explain in an article publish this week in Nature Structure and Molecular Biology , researcher at the Salk Institute for Biological Studies , lead by molecular and cellular telephone biology professor Vicki Lundblad , have discovered how Est3 keeps telomere long each sentence barm cells divide . telomere are made with an enzyme known as telomerase , and Est3 avail bundle extra telomerase onto the ends of freshly - divided chromosomes . Then the telomerase build long telomeres to keep those cells vernal . But what ’s really challenging about all this is that Est3 , which you ’ll recollect is in yeast cell , has an analogue in mammals love as TPP1 . This is where thing get really exciting . If it turns out that TPP1 is involved in keeping our telomere long , scientist can protrude research it and determining whether it could provide a key to maintain humans unseasoned for much longer than ever before . There is a danger , though . As the researcher aim out in a release about their study :

Factors that regulate telomerase bodily process are a very hot subject in biomedicine : sulky telomerase natural action promote previous cell expiry and may underlie diseases of aging via telomere shortening , while hyperactive telomerase could promote uncontrolled cell division and cellular immortality associated with malignant neoplastic disease .

So we do n’t desire too much telomerase , or our cells will go cancerous . But the discovery of Est3 bodes well for anyone who would n’t bear in mind a niggling protein interposition to keep their cell ( and torso ) young . Keeping Cells Useful[Eurekalert via Salk Institute ]

Last Of Us 7 Ellie Crash

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