“TZAP (Telomere Zinc-finger Associated Protein) Trims Telomeres”: TZAP (recently discovered) doesn’t produce Cancer…

Detailed and precise knowledge of how telomeres shorten and lengthen is very important for understanding how we age and how cancer develops. Subsequently, these insights may provide ways to kill immortal cancer cells and safely slow, or even reverse, aging.
Researchers have recently identified a new protein that is involved in controlling the length of telomeres.
They have found that TZAP, short for telomeric zinc finger-associated protein, specifically localizes to telomeres in cells that do and do not express telomerase. TZAP localized to telomeres in similar amounts to TRF1, another protein known to bind telomeres.
TZAP is the first new protein found to localize to telomeres that does not interact with and is not part of the shelterin complex, which helps protect telomeres. Rather, TZAP competes for telomeric binding with members of the shelterin complex, like TRF2.
Long telomeres and short telomeres have the same amount of shelterin complex binding, meaning in long telomeres the density of shelterin binding is lower.
Moreover, when TZAP binds long telomeres in the absence of telomerase, the telomeres rapidly grow shorter in a process known as telomere trimming.
As past studies have shown that telomeric trimming is particularly important in maintaining embryonic stem cell (ESC) telomere length, the researchers wanted to investigate the role of TZAP in these cells.
They deleted TZAP from embryonic stem cells using precise genome editing and found that TZAP-negative cells had much longer telomeres. Reintroducing TZAP to the TZAP-negative ESCs shortened their telomeres.
This study provides additional insight into how telomere length is maintained, a mechanism that could be targeted to help us better understand human lifespan and cancer risk.
....... Dr. H.K.Saboowala.