Telomerase is an enzyme that adds specific DNA sequence repeats ("TTAGGG" in all vertebrates) to the 3' ("three prime") end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes. Enzymes are Biomolecules that catalyze ( ie increase the rates of Chemical reactions Almost all enzymes are Proteins Deoxyribonucleic acid ( DNA) is a Nucleic acid that contains the genetic instructions used in the development and functioning of all known A telomere is a region of repetitive DNA at the end of Chromosomes which protects the end of the chromosome from destruction Animals Plants fungi, and Protists are eukaryotes (juːˈkærɪɒt or -oʊt Organisms whose cells are organized into complex A chromosome is an organized structure of DNA and Protein that is found in cells. The telomeres contain condensed DNA material, giving stability to the chromosomes. The enzyme is a reverse transcriptase that carries its own RNA molecule, which is used as a template when it elongates telomeres, which are shortened after each replication cycle. In Biochemistry, a reverse transcriptase, also known as RNA-dependent DNA polymerase, is a DNA polymerase Enzyme that transcribes Ribonucleic acid ( RNA) is a Nucleic acid that consists of a long chain of Nucleotide units The cell cycle, or cell-division cycle, is the series of events that take place in a eukaryotic cell leading to its replication Telomerase was discovered by Carol W. Greider and Elizabeth Blackburn in 1984 in the ciliate Tetrahymena. Carol Greider is a molecular biologist at Johns Hopkins University, who discovered the enzyme Telomerase in 1984 while working with Elizabeth Elizabeth (Liz Helen Blackburn FRS (b November 26, 1948 in Hobart, Tasmania) is an Australian -born U Tetrahymena are free-living Ciliate Protozoa that can also switch from commensalistic to Pathogenic modes of survival 
The protein composition of human telomerase was identified in 2007 by Dr Scott Cohen and his team at the Children's Medical Research Institute in Australia. The Children's Medical Research Institute ( CMRI) is an Australian based independent scientific research organisation created in the 1950s to "perform scientific  It consists of two molecules each of human Telomerase Reverse Transcriptase (TERT), Telomerase RNA (hTR or TERC) and dyskerin. TERT is an acronym for TE lomerase R everse T ranscriptase a Protein subgroup Telomerase is a Ribonucleoprotein Reverse transcriptase that synthesises telomeric DNA  The two types of protein subunits of the enzyme are coded by two different genes in the genome. In classical genetics the genome of a Diploid Organism including Eukarya refers to a full set of chromosomes or genes in a Gamete, thereby The coding region of the TERT gene is 3396bp, and translates to a protein of 1131 amino acids. In Molecular biology, two Nucleotides on opposite complementary DNA or RNA strands that are connected via Hydrogen bonds are called Proteins are large Organic compounds made of Amino acids arranged in a linear chain and joined together by Peptide bonds between the Carboxyl In Chemistry, an amino acid is a Molecule containing both Amine and Carboxyl Functional groups In Biochemistry, this The polypeptide folds with TERC (451 nucleotides long), which is not translated and remains as RNA. Nucleotides are Organic compounds that consist of three joined structures a nitrogenous base a Sugar, and a Phosphate group Translation is the first stage of Protein biosynthesis (part of the overall process of Gene expression) TERT has a 'mitten' structure that allows it to wrap around the chromosome to add single-stranded telomere repeats.
TERT is a reverse transcriptase, which is a class of enzyme that creates single-stranded DNA using single-stranded RNA as a template. In Biochemistry, a reverse transcriptase, also known as RNA-dependent DNA polymerase, is a DNA polymerase Enzyme that transcribes Enzymes of this class (not TERT specifically, but the ones isolated from viruses) are utilized by scientists in the molecular biological process of Reverse Transcriptase PCR (RT-PCR), which allows the creation of several DNA copies of a target sequence using RNA as a template. A virus (from the Latin virus meaning Toxin or Poison) is a sub-microscopic infectious agent that is unable A scientist, in the broadest sense refers to any person that engages in a systematic activity to acquire Knowledge or an individual that engages in such practices In Molecular biology, reverse transcription polymerase chain reaction (RT-PCR is a Laboratory technique for amplifying a defined piece of a Ribonucleic As stated above, TERT carries its own template around, TERC.
By using TERC, TERT can add a six-nucleotide repeating sequence, 5'-TTAGGG (in all vertebrates, the sequence differs in other organisms) to the 3' strand of chromosomes. These TTAGGG repeats (with their various protein binding partners) are called telomeres. The template region of TERC is 3'-CAAUCCCAAUC-5'. This way, telomerase can bind the first few nucleotides of the template to the last telomere sequence on the chromosome, add a new telomere repeat (5'-GGTTAG-3') sequence, let go, realign the new 3'-end of telomere to the template, and repeat the process. (For an explanation on why this elongation is necessary see Telomere shortening. A telomere is a region of repetitive DNA at the end of Chromosomes which protects the end of the chromosome from destruction )
The enzyme telomerase allows for replacement of short bits of DNA known as a telomere, which are otherwise lost when a cell divides via mitosis. A telomere is a region of repetitive DNA at the end of Chromosomes which protects the end of the chromosome from destruction
In normal circumstances, without the presence of telomerase, if a cell divides recursively, at some point all the progeny will reach their Hayflick limit. The Hayflick limit is the number of times a cell will divide before it stops due to the telomere reaching a critical length. With the presence of telomerase, each dividing cell can replace the lost bit of DNA, and any single cell can then divide unbounded. While this unbounded growth property has excited many researchers, caution is warranted in exploiting this property, as exactly this same unbounded growth is a crucial step in enabling cancerous growth.
Embryonic stem cells express telomerase, which allows them to divide repeatedly and form the individual. Embryonic stem cells (ES cells are Stem cells derived from the inner cell mass of an early stage Embryo known as a Blastocyst. In adults, telomerase is highly expressed in cells that need to divide regularly (e. g. , in the immune system), whereas most somatic cells express it only at very low levels in a cell-cycle dependent manner. "Somatic" redirects here for the musician known as Somatic see Hahn Rowe.
A variety of premature aging syndromes are associated with short telomeres.  These include Werner syndrome, Ataxia telangiectasia, Bloom syndrome, Fanconi anemia, Nijmegen breakage syndrome, and ataxia telangiectasia-like disorder. Werner Syndrome (WRN is a very rare autosomal recessive disorder characterized by the appearance of premature aging. Ataxia-telangiectasia (AT ( Boder-Sedgwick syndrome or Louis-Bar syndrome) is a rare neurodegerative inherited disease which affects many parts of the body Bloom syndrome (BLM is a rare Autosomal Recessive chromosomal disorder characterized by a high frequency of breaks and rearrangements in an affected person's Fanconi anemia (FA is a genetic disease that affects children and adults from all ethnic backgrounds Nijmegen breakage syndrome (NBS (also known as Berlin breakage syndrome and Seemanova syndrome) is a rare syndrome characterised by chromosomal instability probably The genes that have been mutated in these diseases all have roles in the repair of DNA damage, and their precise roles in maintaining telomere length are an active area of investigation. DNA repair refers to a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its Genome. While it is currently unknown to what extent telomere erosion contributes to the normal aging process, maintenance of DNA in general, and telomeric DNA specifically , have emerged as major players. Dr. Michael Fossel has suggested in an interview that telomerase therapies may be used not only to combat cancer but also to actually get around human aging and extend lifespan significantly. Michael B Fossel MD, PhD (born 1950 Greenwich Connecticut) is a professor of Clinical medicine at Michigan State University Cancer (medical term Malignant Neoplasm) is a class of Diseases in which a group of cells display uncontrolled He believes human trials of telomerase-based therapies for extending lifespan will occur within the next 10 years. This timeline is significant because it coincides with the retirement of Baby Boomers in the United States and Europe. Baby boomer is a term used to describe a person who was born during the Post-World War II baby boom between 1946 and 1964 The United States of America —commonly referred to as the
Despite the blatant involvement of telomerase dysfunction in specific genetic pathologies, the link between telomere dysfunction and aging is, at present, profoundly speculative. Telomere shortening may very well have absolutely no role in the etiology of the aging process, and more research is needed to discern whether or not this is the case. In particular, recent research has called into the question the role of telomeres as "cellular clocks" shortening with each division, due to the role of telomeres in mediating other cellular damage processes. Additionally, there is evidence that post-mitotic cells such as neurons undergo cellular aging, yet mitosis-mediated telomere-shortening having a role in this is extraordinarily dubious because these differentiated cells do not divide. Furthermore, even if telomeres were demonstrated to have a role in cellular aging, this does not necessarily translate into anything relevant for the treatment or reversal of organismal aging.
When cells are approaching the Hayflick limit in cell cultures, the time to senescence can be extended by the inactivation of the tumor suppressor proteins - TP53 and Retinoblastoma protein (pRb). The Hayflick limit is the number of times a cell will divide before it stops due to the telomere reaching a critical length. Cell culture is the process by which prokaryotic, or eukaryotic cells are grown under controlled conditions Senescence refers to the biological processes of a living Organism approaching an advanced age (i A tumor suppressor gene, or antioncogene is a Gene that protects a cell from one step on the path to cancer p53 (also known as protein 53 or tumor protein 53) is a Transcription factor encoded by the TP53 gene The retinoblastoma protein (abbreviated pRb or Rb) is a Tumor suppressor Protein that is dysfunctional in many types of Cancer Cells that have been so-altered will eventually undergo an event termed a "crisis" when the majority of the cells in the culture die. The cell is the structural and functional unit of all known living Organisms It is the smallest unit of an organism that is classified as living and is often called Sometimes, a cell does not stop dividing once it reaches crisis. In a typical situation, the telomeres are lost, and the integrity of the chromosomes declines with every subsequent cell division. Exposed chromosome ends are interpreted as double-stranded breaks (DSB) in DNA; such damage is usually repaired by reattaching (religating) the broken ends together. DNA repair refers to a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its Genome. When the cell does this due to telomere-shortening, the ends of different chromosomes can be attached together. This temporarily solves the problem of lacking telomeres; but, during anaphase of cell division, the fused chromosomes are randomly ripped apart, causing many mutations and chromosomal abnormalities. In biology mutations are changes to the Nucleotide sequence of the Genetic material of an organism As this process continues, the cell's genome becomes unstable. Eventually, either sufficient damage will be done to the cell's chromosomes such that cell dies (via programmed cell death, apoptosis), or an additional mutation that activates telomerase will take place.
With the activation of telomerase, some types of cells and their offspring become immortal, that is, their chromosomes will not become unstable no matter how many cell divisions they undergo (they bypass the Hayflick limit), thus avoiding cell death as long as the conditions for their duplication are met. Biological Immortality can be defined as the absence of a sustained increase in rate of mortality as a function of chronological age The Hayflick limit is the number of times a cell will divide before it stops due to the telomere reaching a critical length. Many cancer cells are considered 'immortal' because telomerase activity allows them to divide virtually forever, which is why they can form tumors. Cancer (medical term Malignant Neoplasm) is a class of Diseases in which a group of cells display uncontrolled See also Cancer A tumor or tumour is the name for a swelling or lesion formed by an abnormal growth of cells (termed neoplastic A good example of cancer cells' immortality is HeLa cells, which have been used in laboratories as a model cell line since 1951. A HeLa cell (also Hela or hela cell) is an immortal cell line used in medical research Cell culture is the process by which prokaryotic, or eukaryotic cells are grown under controlled conditions They are indeed immortal - daily production of HeLa cells is estimated at several tons even up to this day.
While this method of modeling human cancer in cell culture is effective and has been used for many years by scientists, it is also very imprecise. The exact changes that allow for the formation of the tumorigenic clones in the above-described experiment are not clear. Cloning in Biology is the process of producing populations of genetically-identical individuals that occurs in nature when organisms such as Bacteria, Insects Scientists have subsequently been able to address this question by the serial introduction of several mutations present in a variety of human cancers. This has led to the elucidation of several combinations of mutations that are sufficient for the formation of tumorigenic cells, in a variety of cell types. While the combination varies depending on the cell type, a common theme is that the following alterations are required: activation of TERT, loss of p53 pathway function, loss of pRb pathway function, activation of the Ras or myc proto-oncogenes, and aberration of the PP2A protein phosphatase. Myc (cMyc is a gene that regulates other genes It codes for a protein that binds to the DNA of other genes An oncogene is a protein encoding Gene, which — when deregulated — participates in the onset and development of Cancer. A phosphatase is an Enzyme that removes a Phosphate group from its Substrate by hydrolysing Phosphoric acid mono Esters into That is to say, the cell has an activated telomerase, eliminating the process of death by chromosome instability or loss, absence of apoptosis-induction pathways, and continued activation of mitosis. Mitosis is the process in which a Eukaryotic cell separates the Chromosomes in its Cell nucleus, into two identical sets in two daughter nuclei
This model of cancer in cell culture accurately describes the role of telomerase in actual human tumors. Cancer (medical term Malignant Neoplasm) is a class of Diseases in which a group of cells display uncontrolled Telomerase activation has been observed in ~90% of all human tumors, suggesting that the immortality conferred by telomerase plays a key role in cancer development. Of the tumors that have not activated TERT, most have found a separate pathway to maintain telomere length termed ALT (Alternative Lengthening of Telomeres). The exact mechanism behind telomere maintenance in the ALT pathway has not been elucidated, but likely involves multiple recombination events at the telomere.
Additional roles for telomerase per work by Dr. Elizabeth Blackburn et al. Elizabeth (Liz Helen Blackburn FRS (b November 26, 1948 in Hobart, Tasmania) is an Australian -born U , include the upregulation of 70 genes known or suspected in cancers' growth and spread through the body, and the activation of glycolysis, which enables cancer cells to rapidly use sugar to facilitate their programmed growth rate. (roughly the growth rate of a fetus)
E. V. Gostjeva et al (MIT) recently imaged colon cancer stem cells and compared them to fetal colon stem cells trying to make a new colon; they were the same.
Dr. Elizabeth Blackburn et al. UCSF has shown work that reveals that mothers caring for their very sick children have shorter telomeres when they report that their emotional stress is at the greatest point. She also found telomerase active at the site of blockages in coronary artery tissue. This could be why heart attacks can come on so suddenly: Telomerase is driving the growth of the blockage.
Other work has shown that the poor of society have shorter telomeres than the rich.  Short telomeres can lead to telomeric crisis and the initiation of cancer if many other conditions are also met, or so the discussion goes at this point.
Dr. Blackburn and the two other co-discoverers of telomerase won the Lasker Prize (2006) for the discovery of telomerase and subsequent work on telomerase. Dr. Blackburn also won the 2006 Gruber Genetics Prize for same. Seventy winners of the Lasker have gone on to be awarded the Nobel.
Mutations in TERT have been implicated in predisposing patients to aplastic anemia, a disorder in which the bone marrow fails to produce blood cells, in 2005. Bone marrow is the flexible tissue found in the hollow interior of Bones In adults marrow in large bones produces new Blood cells It constitutes 4% of 
Cri du chat Syndrome (CdCS) is a complex disorder involving the loss of the distal portion of the short arm of chromosome 5. Cri du Chat syndrome or Cri-du-Chat syndrome (French for Cry or call of the cat referring to the specific cry of the child also called TERT is located in the deleted region, and loss of one copy of TERT has been suggested as a cause or contributing factor of this disease. 
Dyskeratosis congenita (DC) is a disease of the bone marrow that can be caused by a mutation in the telomerase RNA subunit, TERC. Dyskeratosis congenita (DKC also called Zinsser-Cole-Engman syndrome, is a rare progressive Congenital disorder of the Integumentary system that also Bone marrow is the flexible tissue found in the hollow interior of Bones In adults marrow in large bones produces new Blood cells It constitutes 4% of Mutation of TERC accounts for only 5% of all cases, and, when DC occurs by this mutation, it is inherited as an autosomal dominant disorder. Mutations in the gene Dyskerin (DKC1) account for about 35% of DC cases, and, in this case, the inheritance pattern is X-linked-recessive.
Patients with DC have severe bone marrow failure manifesting as abnormal skin pigmentation, leucoplakia (a white thickening of the oral mucosa), and nail dystophy, as well as a variety of other symptoms. Human skin color can range from almost black (due to very high concentrations of the dark brown pigment melanin to nearly colorless (appearing reddish white due to the Blood Leukoplakia is adherent white plaques or patches on the mucous membranes of the oral cavity including the Tongue. Individuals with either TERC or DKC1 mutations have shorter telomeres and defective telomerase activity in vitro than other individuals of the same age. 
There has also been one family in which autosomal dominant DC has been linked to a heterozygous mutation in TERT.  These patients also exhibited an increased rate of telomere-shortening, and genetic anticipation (i. e. , the DC phenotype worsened with each generation).
Cancer is a very difficult disease to fight because the immune system has trouble recognizing it, and cancer cells are immortal; they will always continue dividing. Because telomerase is necessary for the immortality of so many cancer types, it is thought to be a potential drug target. A drug, broadly speaking is any chemical substance that when absorbed into the body If a drug can be used to turn off telomerase in cancer cells, the above process of telomere-shortening will resume—telomere length will be lost as the cells continue to divide, mutations will occur, and cell stability will decrease. Experimental drug and vaccine therapies targeting active telomerase have been tested in mouse models, and some have now entered early clinical trials. Geron Corporation is currently conducting four human clinical trials involving telomerase inhibition and telomerase vaccination. Geron Corporation is a biotechnology company founded by Dr Michael D Merck, as a licensee of Geron, has recent approval of an IND for one vaccine type. The vaccine platform is being tested (and now jointly with Merck) using three different approaches. One vaccine is adenovirus/plasmid based (Merck IND). The second is an autologous dendritic cell based vaccine (GRNVAC1), formerly called TVAX when tested in Phase I clinical trials in Prostate Cancer, and it showed significant PSA doubling times as well as T-cell response. Geron's embryonic stem cell derived dendritic cell vaccine targeting telomerase is the third approach and is currently at the pre-clinical stage. These vaccine methods attempt to teach the human immune system to attack cancer cells expressing telomerase. Geron's telomerase inhibitor drug (GRN163L) attempts to stop cancer cell proliferation by inhibiting telomerase and it is in three separate early stage human clinical trials. Indeed, telomerase inhibition in many types of cancer cells grown in culture has led to the massive death of the cell population. However, a variety of caveats, including the presence of the ALT pathway, complicate such therapies. A telomere is a region of repetitive DNA at the end of Chromosomes which protects the end of the chromosome from destruction Some have reported ALT methods of telomere maintenance and storage of DNA in cancer stem cells, however Geron claims to have killed cancer stem cells with their telomerase inhibitor GRN163L at Johns Hopkins. GRN163L binds directly to the RNA template of telomerase. Even a mutation of the RNA template of telomerase would render the telomerase unable to extend telomeres, and therefore not be able to grant replicative immortality to cancer, not allow glycolysis to be inititated, and not upregulate Blackburn's 70 cancer genes. Since Blackburn has shown that most of the harmful cancer-related effects of telomerase are dependent on an intact RNA template, it seems a very worthwhile target for drug development. If indeed some cancer stem cells use an alternative method of telomere maintenance, it should be noted that they are still killed when the RNA template of telomerase is blocked. According to Blackburn's opinion at most of her lectures, it is a big mistake to think that telomerase is involved with only extending telomeres. Stopping glycolysis in cancer stem cells and preventing the upregulation of 70 bad genes is probably what is killing cancer stem cells if they are using alternative methods.
Guenther Witzany (2007). "Telomeres in Evolution and Development from Biosemiotic Perspective". Nature Precedings. doi: . A digital object identifier ( DOI) is a permanent identifier given to an Electronic document.