paper<\/a> published in January 2023, the team mapped more than 300 serine\/threonine kinases, the other main type of protein kinase, to their motifs. In the current paper, they complete the human \u201ckinome\u201d by successfully mapping 93 tyrosine kinases to their corresponding motifs.<\/p>\nNext, by creating and using advanced computational tools, Yaron-Barir, Krismer, Joughin, Takegami, and Yaffe tested whether the results were predictive of real proteins, and whether the results might reveal unknown signaling events in normal and cancer cells. By analyzing phosphoproteomic data from mass spectrometry to reveal phosphorylation patterns in cells, their atlas accurately predicted tyrosine kinase activity in previously studied cell signaling pathways.<\/p>\n
For example, using recently published phosphoproteomic data of human lung cancer cells treated with two targeted drugs, the atlas identified that treatment with erlotinib, a known inhibitor of the protein EGFR, downregulated sites matching a motif for EGFR. Treatment with afatinib, a known HER2 inhibitor, downregulated sites matching the HER2 motif. Unexpectedly, afatinib treatment also upregulated the motif for the tyrosine kinase MET, a finding that helps explain patient data linking MET activity to afatinib drug resistance.<\/p>\n
Actionable results<\/strong><\/p>\nThere are two key ways researchers can use the new atlas. First, for a protein of interest that is being phosphorylated, the atlas can be used to narrow down hundreds of kinases to a short list of candidates likely to be involved. \u201cThe predictions that come from using this will still need to be validated experimentally, but it\u2019s a huge step forward in making clear predictions that can be tested,\u201d says Yaffe.<\/p>\n
Second, the atlas makes phosphoproteomic data more useful and actionable. In the past, researchers might gather phosphoproteomic data from a tissue sample, but it was difficult to know what that data was saying or how to best use it to guide next steps in research. Now, that data can be used to predict which kinases are upregulated or downregulated and therefore which cellular signaling pathways are active or not.<\/p>\n
\u201cWe now have a new tool now to interpret those large datasets, a Rosetta Stone for phosphoproteomics,\u201d says Yaffe. \u201cIt is going to be particularly helpful for turning this type of disease data into actionable items.\u201d<\/p>\n
In the context of cancer, phosophoproteomic data from a patient\u2019s tumor biopsy could be used to help doctors quickly identify which kinases and cell signaling pathways are involved in cancer expansion or drug resistance, then use that knowledge to target those pathways with appropriate drug therapy or combination therapy.<\/p>\n
Yaffe\u2019s lab and their colleagues at the National Institutes of Health are now using the atlas to seek out new insights into difficult cancers, including appendiceal cancer and neuroendocrine tumors. While many cancers have been shown to have a strong genetic component, such as the genes BRCA1 and BRCA2\u00a0in breast cancer, other cancers are not associated with any known genetic cause. \u201cWe\u2019re using this atlas to interrogate these tumors that don\u2019t seem to have a clear genetic driver to see if we can identify kinases that are driving cancer progression,\u201d he says.<\/p>\n
Biological insights<\/strong><\/p>\nIn addition to completing the human kinase atlas, the team made two biological discoveries in their recent study. First, they identified three main classes of phosphorylation motifs, or barcodes, for tyrosine kinases. The first class is motifs that map to multiple kinases, suggesting that numerous signaling pathways converge to phosphorylate a protein boasting that motif. The second class is motifs with a one-to-one match between motif and kinase, in which only a specific kinase will activate a protein with that motif. This came as a partial surprise, as tyrosine kinases have been thought to have minimal specificity by some in the field.<\/p>\n
The final class includes motifs for which there is no clear match to one of the 78 classical tyrosine kinases. This class includes motifs that match to 15 atypical tyrosine kinases known to also phosphorylate serine or threonine residues. \u201cThis means that there\u2019s a subset of kinases that we didn\u2019t recognize that are actually playing an important role,\u201d says Yaffe. It also indicates there may be other mechanisms besides motifs alone that affect how a kinase interacts with a protein.<\/p>\n
The team also discovered that tyrosine kinase motifs are tightly conserved between humans and the worm species C. elegans,\u00a0<\/em>despite the species being separated by more than 600 million years of evolution. In other words, a worm kinase and its human homologue are phosphorylating essentially the same motif. That sequence preservation suggests that tyrosine kinases are highly critical to signaling pathways in all multicellular organisms, and any small change would be harmful to an organism.<\/p>\nThe research was funded by the Charles and Marjorie Holloway Foundation, the MIT Center for Precision Cancer Medicine, the Koch Institute Frontier Research Program via L. Scott Ritterbush, the Leukemia and Lymphoma Society, the National Institutes of Health, Cancer Research UK, the Brain Tumour Charity, and the Koch Institute Support (core) grant from the National Cancer Institute.<\/p>\n","protected":false},"excerpt":{"rendered":"
A newly complete database of human protein kinases and their preferred binding sites provides a powerful new platform to investigate cell signaling pathways. Culminating 25 years of research, MIT, Harvard University, and Yale University scientists and collaborators have unveiled a comprehensive atlas of human tyrosine kinases \u2014 enzymes that regulate a wide variety of cellular […]<\/p>\n","protected":false},"author":1,"featured_media":29187,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[6229,6250,6212],"tags":[],"class_list":["post-29185","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-koch-institute","category-koch-institute-faculty-locations","category-news-briefs","placement-placement-homepage","research-area-biochemistry-biophysics-and-structural-biology","research-area-cancer-biology","research-area-computational-biology"],"acf":[],"yoast_head":"\n
\u201cRosetta Stone\u201d of cell signaling could expedite precision cancer medicine - MIT Department of Biology<\/title>\n \n \n \n \n \n \n \n \n \n \n \n\t \n\t \n\t \n \n \n \n\t \n\t \n\t \n