Changes in 8dbfa5e: update bib

				morinlab.bib
			
          @@ -1,3 +1,21 @@

          +@article{almasmoumFrequentLossBTG12021,

          +  title = {Frequent Loss of {{BTG1}} Activity and Impaired Interactions with the {{Caf1}} Subunit of the {{Ccr4-Not}} Deadenylase in Non-{{Hodgkin}} Lymphoma},

          +  author = {Almasmoum, Hibah Ali and Airhihen, Blessing and Seedhouse, Claire and Winkler, Gerlof Sebastiaan},

          +  date = {2021-02},

          +  journaltitle = {Leukemia \& Lymphoma},

          +  shortjournal = {Leuk Lymphoma},

          +  volume = {62},

          +  number = {2},

          +  eprint = {33021411},

          +  eprinttype = {pmid},

          +  pages = {281--290},

          +  issn = {1029-2403},

          +  doi = {10.1080/10428194.2020.1827243},

          +  abstract = {Mutations in the highly similar genes B-cell translocation gene 1 (BTG1) and BTG2 are identified in approximately 10-15\% of non-Hodgkin lymphoma cases, which may suggest a direct involvement of BTG1 and BTG2 in malignant transformation. However, it is unclear whether or how disease-associated mutations impair the function of these genes. Therefore, we selected 16 BTG1 variants based on in silico analysis. We then evaluated (i) the ability of these variants to interact with the known protein-binding partners CNOT7 and CNOT8, which encode the Caf1 catalytic subunit of the Ccr4-Not deadenylase complex; (ii) the activity of the variant proteins in cell cycle progression; (iii) translational repression; and (iv) mRNA degradation. Based on these analyses, we conclude that mutations in BTG1 may contribute to malignant transformation and tumor cell proliferation by interfering with its anti-proliferative activity and ability to interact with CNOT7 and CNOT8.},

          +  langid = {english},

          +  keywords = {BTG1,BTG2,Ccr4–Not,Cell Proliferation,Exoribonucleases,Humans,Immediate-Early Proteins,Lymphoma and Hodgkin disease,Lymphoma Non-Hodgkin,mRNA decay,Neoplasm Proteins,Protein Binding,Receptors CCR4,Repressor Proteins,Transcription Factors,Tumor Suppressor Proteins},

          +}

          +

           @article{wanMechanismActivationRAFERK2004,

             title = {Mechanism of Activation of the {{RAF-ERK}} Signaling Pathway by Oncogenic Mutations of {{B-RAF}}},

             author = {Wan, Paul T. C. and Garnett, Mathew J. and Roe, S. Mark and Lee, Sharlene and Niculescu-Duvaz, Dan and Good, Valerie M. and Jones, C. Michael and Marshall, Christopher J. and Springer, Caroline J. and Barford, David and Marais, Richard and {Cancer Genome Project}},

...	...	@@ -1,3 +1,21 @@
	1	+@article{almasmoumFrequentLossBTG12021,
	2	+ title = {Frequent Loss of {{BTG1}} Activity and Impaired Interactions with the {{Caf1}} Subunit of the {{Ccr4-Not}} Deadenylase in Non-{{Hodgkin}} Lymphoma},
	3	+ author = {Almasmoum, Hibah Ali and Airhihen, Blessing and Seedhouse, Claire and Winkler, Gerlof Sebastiaan},
	4	+ date = {2021-02},
	5	+ journaltitle = {Leukemia \& Lymphoma},
	6	+ shortjournal = {Leuk Lymphoma},
	7	+ volume = {62},
	8	+ number = {2},
	9	+ eprint = {33021411},
	10	+ eprinttype = {pmid},
	11	+ pages = {281--290},
	12	+ issn = {1029-2403},
	13	+ doi = {10.1080/10428194.2020.1827243},
	14	+ abstract = {Mutations in the highly similar genes B-cell translocation gene 1 (BTG1) and BTG2 are identified in approximately 10-15\% of non-Hodgkin lymphoma cases, which may suggest a direct involvement of BTG1 and BTG2 in malignant transformation. However, it is unclear whether or how disease-associated mutations impair the function of these genes. Therefore, we selected 16 BTG1 variants based on in silico analysis. We then evaluated (i) the ability of these variants to interact with the known protein-binding partners CNOT7 and CNOT8, which encode the Caf1 catalytic subunit of the Ccr4-Not deadenylase complex; (ii) the activity of the variant proteins in cell cycle progression; (iii) translational repression; and (iv) mRNA degradation. Based on these analyses, we conclude that mutations in BTG1 may contribute to malignant transformation and tumor cell proliferation by interfering with its anti-proliferative activity and ability to interact with CNOT7 and CNOT8.},
	15	+ langid = {english},
	16	+ keywords = {BTG1,BTG2,Ccr4–Not,Cell Proliferation,Exoribonucleases,Humans,Immediate-Early Proteins,Lymphoma and Hodgkin disease,Lymphoma Non-Hodgkin,mRNA decay,Neoplasm Proteins,Protein Binding,Receptors CCR4,Repressor Proteins,Transcription Factors,Tumor Suppressor Proteins},
	17	+}
	18	+
1	19	@article{wanMechanismActivationRAFERK2004,
2	20	title = {Mechanism of Activation of the {{RAF-ERK}} Signaling Pathway by Oncogenic Mutations of {{B-RAF}}},
3	21	author = {Wan, Paul T. C. and Garnett, Mathew J. and Roe, S. Mark and Lee, Sharlene and Niculescu-Duvaz, Dan and Good, Valerie M. and Jones, C. Michael and Marshall, Christopher J. and Springer, Caroline J. and Barford, David and Marais, Richard and {Cancer Genome Project}},