Changes in 92ff078: more fixes

				morinlab.bib
			
          @@ -1,3 +1,23 @@

          +@article{saffieFBXW7TriggersDegradation2020b,

          +  title = {{{FBXW7 Triggers Degradation}} of {{KMT2D}} to {{Favor Growth}} of {{Diffuse Large B-cell Lymphoma Cells}}},

          +  author = {Saffie, Rizwan and Zhou, Nan and Rolland, Delphine and Önder, Özlem and Basrur, Venkatesha and Campbell, Sydney and Wellen, Kathryn E. and Elenitoba-Johnson, Kojo S. J. and Capell, Brian C. and Busino, Luca},

          +  date = {2020-06-15},

          +  journaltitle = {Cancer Research},

          +  shortjournal = {Cancer Res},

          +  volume = {80},

          +  number = {12},

          +  eprint = {32350066},

          +  eprinttype = {pmid},

          +  pages = {2498--2511},

          +  issn = {1538-7445},

          +  doi = {10.1158/0008-5472.CAN-19-2247},

          +  abstract = {Mature B-cell neoplasms are the fifth most common neoplasm. Due to significant heterogeneity at the clinical and genetic levels, current therapies for these cancers fail to provide long-term cures. The clinical success of proteasome inhibition for the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin pathway an important emerging therapeutic target. In this study, we assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. FBXW7 targeted the frequently inactivated tumor suppressor KMT2D for protein degradation, subsequently regulating gene expression signatures related to oxidative phosphorylation (OxPhos). Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxPhos inhibition. These data elucidate a novel mechanism of regulation of KMT2D levels by the ubiquitin pathway and uncover a role of FBXW7 in regulating oxidative phosphorylation in B-cell malignancies. SIGNIFICANCE: These findings characterize FBXW7 as a prosurvival factor in B-cell lymphoma via degradation of the chromatin modifier KMT2D.},

          +  langid = {english},

          +  pmcid = {PMC7417195},

          +  keywords = {Animals,Cell Line Tumor,Cell Proliferation,Chromatin,DNA-Binding Proteins,F-Box-WD Repeat-Containing Protein 7,Female,Gene Expression Regulation Neoplastic,Gene Knockout Techniques,HEK293 Cells,Humans,Lymphoma Large B-Cell Diffuse,Mice,Neoplasm Proteins,Oxidative Phosphorylation,Proteolysis,RNA Small Interfering,Signal Transduction,Ubiquitin,Xenograft Model Antitumor Assays},

          +  file = {/Users/rmorin/Zotero/storage/5KJ466DP/Saffie et al. - 2020 - FBXW7 Triggers Degradation of KMT2D to Favor Growt.pdf;/Users/rmorin/Zotero/storage/RQSU3BV9/Saffie et al. - 2020 - FBXW7 Triggers Degradation of KMT2D to Favor Growt.pdf}

          +}

          +

           @article{katoUnderstandingFunctionstructureFunctionmutation2003,

             title = {Understanding the Function-Structure and Function-Mutation Relationships of P53 Tumor Suppressor Protein by High-Resolution Missense Mutation Analysis},

             author = {Kato, Shunsuke and Han, Shuang-Yin and Liu, Wen and Otsuka, Kazunori and Shibata, Hiroyuki and Kanamaru, Ryunosuke and Ishioka, Chikashi},

...	...	@@ -1,3 +1,23 @@
	1	+@article{saffieFBXW7TriggersDegradation2020b,
	2	+ title = {{{FBXW7 Triggers Degradation}} of {{KMT2D}} to {{Favor Growth}} of {{Diffuse Large B-cell Lymphoma Cells}}},
	3	+ author = {Saffie, Rizwan and Zhou, Nan and Rolland, Delphine and Önder, Özlem and Basrur, Venkatesha and Campbell, Sydney and Wellen, Kathryn E. and Elenitoba-Johnson, Kojo S. J. and Capell, Brian C. and Busino, Luca},
	4	+ date = {2020-06-15},
	5	+ journaltitle = {Cancer Research},
	6	+ shortjournal = {Cancer Res},
	7	+ volume = {80},
	8	+ number = {12},
	9	+ eprint = {32350066},
	10	+ eprinttype = {pmid},
	11	+ pages = {2498--2511},
	12	+ issn = {1538-7445},
	13	+ doi = {10.1158/0008-5472.CAN-19-2247},
	14	+ abstract = {Mature B-cell neoplasms are the fifth most common neoplasm. Due to significant heterogeneity at the clinical and genetic levels, current therapies for these cancers fail to provide long-term cures. The clinical success of proteasome inhibition for the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin pathway an important emerging therapeutic target. In this study, we assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. FBXW7 targeted the frequently inactivated tumor suppressor KMT2D for protein degradation, subsequently regulating gene expression signatures related to oxidative phosphorylation (OxPhos). Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxPhos inhibition. These data elucidate a novel mechanism of regulation of KMT2D levels by the ubiquitin pathway and uncover a role of FBXW7 in regulating oxidative phosphorylation in B-cell malignancies. SIGNIFICANCE: These findings characterize FBXW7 as a prosurvival factor in B-cell lymphoma via degradation of the chromatin modifier KMT2D.},
	15	+ langid = {english},
	16	+ pmcid = {PMC7417195},
	17	+ keywords = {Animals,Cell Line Tumor,Cell Proliferation,Chromatin,DNA-Binding Proteins,F-Box-WD Repeat-Containing Protein 7,Female,Gene Expression Regulation Neoplastic,Gene Knockout Techniques,HEK293 Cells,Humans,Lymphoma Large B-Cell Diffuse,Mice,Neoplasm Proteins,Oxidative Phosphorylation,Proteolysis,RNA Small Interfering,Signal Transduction,Ubiquitin,Xenograft Model Antitumor Assays},
	18	+ file = {/Users/rmorin/Zotero/storage/5KJ466DP/Saffie et al. - 2020 - FBXW7 Triggers Degradation of KMT2D to Favor Growt.pdf;/Users/rmorin/Zotero/storage/RQSU3BV9/Saffie et al. - 2020 - FBXW7 Triggers Degradation of KMT2D to Favor Growt.pdf}
	19	+}
	20	+
1	21	@article{katoUnderstandingFunctionstructureFunctionmutation2003,
2	22	title = {Understanding the Function-Structure and Function-Mutation Relationships of P53 Tumor Suppressor Protein by High-Resolution Missense Mutation Analysis},
3	23	author = {Kato, Shunsuke and Han, Shuang-Yin and Liu, Wen and Otsuka, Kazunori and Shibata, Hiroyuki and Kanamaru, Ryunosuke and Ishioka, Chikashi},