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C. asiatica has been shown to activate telomerase more than any other known compound yet discovered: 8.8-fold. This exceeds the activation by other known telomerase activators: oleanolic acid 5.9-fold, Astragalus extract 4.3-fold, TA-65 2.2-fold, and maslinic acid 2-fold. [17]
Oleanolic acid activates telomerase in peripheral blood mononuclear cells (PBMCs) 5.9-fold, more than any other compounded tested, with the exception of Centella asiatica (8.8-fold). [14] Less telomerase activation is seen for Astragalus extract 4.3-fold, TA-65 2.2-fold, and maslinic acid 2-fold. [14]
TERRA-Telomerase Interaction at Long Telomeres. At cells with long telomeres, TERRA is proposed to act as a negative regulator of telomerase activity. This direct inhibitor function acts through base-pairing of the tandem repeats found throughout TERRA's 3'-end to the complementary RNA template region of telomerase. [6]
The functionality and efficiency of a reprogrammed iPS cell is determined by the ability of the cell to re-activate the telomerase complex and elongate its telomeres allowing for self-renewal. hTERT is a major limiting component of the telomerase complex and a deficiency of intact hTERT impedes the activity of telomerase, making iPS cells an ...
In most multicellular eukaryotic organisms, telomerase is active only in germ cells, some types of stem cells such as embryonic stem cells, and certain white blood cells. [9] Telomerase can be reactivated and telomeres restored to the embryonic state by somatic cell nuclear transfer. [18]
Telomerase RNA component, also known as TR, TER or TERC, is an ncRNA found in eukaryotes that is a component of telomerase, the enzyme used to extend telomeres. [ 3 ] [ 4 ] TERC serves as a template for telomere replication ( reverse transcription ) by telomerase.
Two concerns with applying telomerase inhibitors in cancer treatment are that effective treatment requires continuous, long-term drug application and that off-target effects are common. [30] For example, the telomerase inhibitor imetelstat, first proposed in 2003, [31] [32] has been held up in clinical trials due to hematological toxicity. [30]
TERF1 may reduce the accessibility of telomerase towards the end of the DNA length, which results in its inhibition. There may be potential post-translation modifications of TERF1 by adding ribose to induce regulation of telomerase. After the lengthening of the telomere, TERF1 reassembles to form an inaccessible T-loop structure. [10]