Nucleotide Metabolism
Nucleotide Metabolism - Related Videos
11:29
HPLC-based Assay to Monitor Extracellular Nucleotide/Nucleoside Metabolism in Human Chronic Lymphocytic Leukemia Cells
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Cited by 5 •
2016
The protocol described here represents an easy and reproducible method that employs reverse phase high-performance liquid chromatography (RP-HPLC) to measure purine metabolism on chronic lymphocytic leukemia (CLL) cells cultured under different conditions.
06:38
Plant Sample Preparation for Nucleoside/Nucleotide Content Measurement with An HPLC-MS/MS
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Cited by 3 •
2021
A precise and reproducible method for in vivo nucleosides/nucleotides quantification in plants is described here. This method employs an HPLC-MS/MS.
05:41
Metabolic Profile Analysis of Zebrafish Embryos
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Cited by 42 •
2013
Zebrafish represent a powerful vertebrate model that has been under-utilised for metabolic studies. Here we describe a rapid way to measure the in vivo metabolic profile of developing zebrafish that allows the comparison of different mitochondrial function parameters between genetically or pharmacologically manipulated embryos, thereby increasing the applicability of this organism.
00:52
What is Metabolism?
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2019
Overview Metabolism represents all of the chemical activity in a cell, including reactions that build molecules (anabolism) and those that break molecules down (catabolism). Anabolic reactions require energy, whereas catabolic reactions provide it. Thus, metabolism describes how cells transform energy through a variety of chemical reactions, which are often made more efficient with the help of enzymes. Metabolism Is the Sum of All of the Chemical Reactions That Take Place in an Organism
01:46
Nucleotide Excision Repair
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2020
Exposure to mutagens can damage DNA and result in bulky lesions that distort the double-helix structure or impede proper transcription. Damaged DNA can be detected and repaired in a process called nucleotide excision repair (NER). NER employs a set of specialized proteins that first scan DNA to detect a damaged region. Next, NER proteins separate the strands and excise the damaged area. Finally, they coordinate the replacement with new, matching nucleotides.DNA distortion and damageCells are...
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Rapidly dividing cancer cells require coordinated nucleotide production to support genome duplication and repair. If purine or pyrimidine availability does not match demand, the processes needed for copying and maintaining DNA may be affected. Studying this balance helps researchers connect altered growth signals with metabolic flux and determine how nucleotide supply contributes to tumor biology.
Ribonucleotide reduction converts ribonucleotides into deoxyribonucleotides, supplying the forms required for DNA replication. This reaction links RNA-related nucleotide pools to the production of DNA building blocks and therefore represents an important control point in proliferating cells. Its central position also makes ribonucleotide reductase a useful enzyme to investigate when examining cancer-associated metabolic vulnerabilities.
De novo synthesis builds nucleotides from small precursors, whereas salvage recovers preformed bases for reuse. These routes give cells alternative ways to maintain purine and pyrimidine pools as metabolic demand changes. Comparing their contributions can help researchers assess how altered growth signals reshape nucleotide flux in cancer and identify which parts of the network may represent vulnerabilities.
Mapping the pathways shows how synthesis, salvage, interconversion, reduction, and degradation contribute to nucleotide availability in tumor cells. This organization helps researchers relate metabolic flux to the demands of genome duplication and repair. It can also guide the identification of metabolic vulnerabilities and support evaluation of interventions directed at specific pathway enzymes.
Thymidylate synthase and ribonucleotide reductase participate in reactions that help supply nucleotides needed for DNA production. Inhibiting these enzymes allows researchers to test whether cancer-associated nucleotide demand creates a metabolic weakness. Such studies can evaluate therapeutic effects while also examining how changes in pathway activity influence tumor responses and the emergence of drug resistance.
Changes in nucleotide pathways can reveal how tumor cells adapt their metabolic flux when growth demands or therapeutic pressures change. Researchers can use this information to relate pathway activity to genome duplication, DNA repair, and treatment response. Comparing these relationships helps characterize tumor biology and supports investigations into why resistance develops during therapies targeting nucleotide-producing enzymes.