UniProt: A worldwide hub of protein knowledge

https://www.cell.com/cell-metabolism/pdf/S1550-4131(15)00621-X.pdf

The Emerging Hallmarks of Cancer Metabolism

Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate

Cancer epigenetics: from mechanism to therapy.

Otto Warburg pioneered quantitative investigations of cancer cell metabolism, as well as photosynthesis and respiration. Warburg and co-workers showed in the 1920s that, under aerobic conditions, tumour tissues metabolize approximately tenfold more glucose to lactate in a given time than normal tissues, a phenomenon known as the Warburg effect. However, this increase in aerobic glycolysis in cancer cells is often erroneously thought to occur instead of mitochondrial respiration and has been misinterpreted as evidence for damage to respiration instead of damage to the regulation of glycolysis. In fact, many cancers exhibit the Warburg effect while retaining mitochondrial respiration. We re-examine Warburg's observations in relation to the current concepts of cancer metabolism as being intimately linked to alterations of mitochondrial DNA, oncogenes and tumour suppressors, and thus readily exploitable for cancer therapy.

Otto Warburg's contributions to current concepts of cancer metabolism

http://basicmed.med.ncku.edu.tw/admin/up_img/1007-2.pdf

Oncometabolite 2-Hydroxyglutarate Is a Competitive Inhibitor of α-Ketoglutarate-Dependent Dioxygenases

Structural Basis for Cooperative Function of Mettl3 and Mettl14 Methyltransferases.

https://www.cell.com/cell/pdf/S0092-8674(13)01469-4.pdf

Crystal Structure of TET2-DNA Complex: Insight into TET-Mediated 5mC Oxidation

The Yes-associated protein (YAP) transcriptional coactivator is a key regulator of organ size and a candidate human oncogene inhibited by the Hippo tumor suppressor pathway. The TEAD family of transcription factors binds directly to and mediates YAP-induced gene expression. Here we report the three-dimensional structure of the YAP (residues 50-171)-TEAD1 (residues 194-411) complex, in which YAP wraps around the globular structure of TEAD1 and forms extensive interactions via three highly conserved interfaces. Interface 3, including YAP residues 86-100, is most critical for complex formation. Our study reveals the biochemical nature of the YAP-TEAD interaction, and provides a basis for pharmacological intervention of YAP-TEAD hyperactivation in human diseases.

http://genesdev.cshlp.org/content/24/3/235.full.pdf

Structural insights into the YAP and TEAD complex

https://www.cell.com/cancer-cell/pdf/S1535-6108(13)00068-8.pdf

Ping Wang

Papers

Oncometabolite 2-Hydroxyglutarate Is a Competitive Inhibitor of α-Ketoglutarate-Dependent Dioxygenases

Structural Basis for Cooperative Function of Mettl3 and Mettl14 Methyltransferases.

Crystal Structure of TET2-DNA Complex: Insight into TET-Mediated 5mC Oxidation

Structural insights into the YAP and TEAD complex

Lysine-5 acetylation negatively regulates lactate dehydrogenase a and is decreased in pancreatic cancer