Azman MS, et al. (2023) An ERK1/2-driven RNA-binding switch in nucleolin drives ribosome biogenesis and pancreatic tumorigenesis downstream of RAS oncogene. EMBO J, e110902 37039106

This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.

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T360-p - CK2A1 (mouse) ▲

Modsite: SGISSVPtPsPLGPL SwissProt Entrez-Gene Orthologous residues CK2A1 (human): T360‑p, CK2A1 (mouse): T360‑p, CK2A1 (rat): T360‑p, CK2A1 (rabbit): T360‑p, CK2A1 (cow): T360‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'pancreatic, ductal'-pancreas Cellular systems studied:  primary cells, tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes KRas (human) increase G12D mutant Trametinib KRas (human) inhibit treatment-induced increase

S362-p - CK2A1 (mouse) ▲

Modsite: ISSVPtPsPLGPLAG SwissProt Entrez-Gene Orthologous residues CK2A1 (human): S362‑p, CK2A1 (mouse): S362‑p, CK2A1 (rat): S362‑p, CK2A1 (rabbit): S362‑p, CK2A1 (cow): S362‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'pancreatic, ductal'-pancreas Cellular systems studied:  primary cells, tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes KRas (human) increase G12D mutant Trametinib KRas (human) inhibit treatment-induced increase

S28-p - NCL (mouse) ▲

Modsite: PKEVEEDsEDEEMsE SwissProt Entrez-Gene Orthologous residues NCL (human): S28‑p, NCL (mouse): S28‑p, NCL (rat): S28‑p, NCL iso6 (rat): S28‑p, NCL (cow): S28‑p Characterization Methods used to characterize site in vivo:  electrophoretic mobility shift, mass spectrometry, mutation of modification site Relevant cell lines - cell types - tissues:  'pancreatic, ductal'-pancreas Cellular systems studied:  primary cells, tissue Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CK2A1 (human) pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes KRas (human) increase G12D mutant Trametinib KRas (human) inhibit treatment-induced increase silmitasertib KRas (human) inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  carcinogenesis, induced, cell growth, induced, transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces

S34-p - NCL (mouse) ▲

Modsite: DsEDEEMsEDEDDss SwissProt Entrez-Gene Orthologous residues NCL (human): S34‑p, NCL (mouse): S34‑p, NCL (rat): S34‑p, NCL iso6 (rat): S34‑p, NCL (cow): S34‑p Characterization Methods used to characterize site in vivo:  electrophoretic mobility shift, mass spectrometry, mutation of modification site Relevant cell lines - cell types - tissues:  'pancreatic, ductal'-pancreas Cellular systems studied:  primary cells, tissue Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CK2A1 (human) pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes KRas (human) increase G12D mutant Trametinib KRas (human) inhibit treatment-induced increase silmitasertib KRas (human) inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  carcinogenesis, induced, cell growth, induced, transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces

S40-p - NCL (mouse) ▲

Modsite: MsEDEDDssGEEEVV SwissProt Entrez-Gene Orthologous residues NCL (human): D40‑p, NCL (mouse): S40‑p, NCL (rat): S40‑p, NCL iso6 (rat): S40‑p, NCL (cow): E40‑p Characterization Methods used to characterize site in vivo:  electrophoretic mobility shift, mass spectrometry, mutation of modification site Relevant cell lines - cell types - tissues:  'pancreatic, ductal'-pancreas Cellular systems studied:  primary cells, tissue Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CK2A1 (human) pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes KRas (human) increase G12D mutant Trametinib KRas (human) inhibit treatment-induced increase silmitasertib KRas (human) inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  carcinogenesis, induced, cell growth, induced, transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces

S41-p - NCL (mouse) ▲

Modsite: sEDEDDssGEEEVVI SwissProt Entrez-Gene Orthologous residues NCL (human): S41‑p, NCL (mouse): S41‑p, NCL (rat): S41‑p, NCL iso6 (rat): S41‑p, NCL (cow): S41‑p Characterization Methods used to characterize site in vivo:  electrophoretic mobility shift, mass spectrometry, mutation of modification site Relevant cell lines - cell types - tissues:  'pancreatic, ductal'-pancreas Cellular systems studied:  primary cells, tissue Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CK2A1 (human) pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes KRas (human) increase G12D mutant Trametinib KRas (human) inhibit treatment-induced increase silmitasertib KRas (human) inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  carcinogenesis, induced, cell growth, induced, transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces