Sathish K.R. Padi
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View article: Cryo-EM structures of PP2A:B55 with p107 and Eya3 define substrate recruitment
Cryo-EM structures of PP2A:B55 with p107 and Eya3 define substrate recruitment Open
Phosphoprotein phosphatases (PPPs) achieve specificity by binding substrates and regulators using PPP-specific short motifs. Protein phosphatase 2A (PP2A) is a highly conserved phosphatase that regulates cell signaling and is a tumor suppr…
View article: Combining cryo-electron microscopy (cryo-EM) with orthogonal solution state methods to define the molecular basis of the phosphoprotein phosphatase family regulation and substrate specificity
Combining cryo-electron microscopy (cryo-EM) with orthogonal solution state methods to define the molecular basis of the phosphoprotein phosphatase family regulation and substrate specificity Open
Protein phosphatases are dynamic enzymes that exhibit complex regulatory mechanisms, with disruptions in these regulatory processes associated with disease. It is now clear that many phosphatases assemble into large macromolecular complexe…
View article: Cryo-EM structures of PP2A:B55–FAM122A and PP2A:B55–ARPP19
Cryo-EM structures of PP2A:B55–FAM122A and PP2A:B55–ARPP19 Open
Progression through the cell cycle is controlled by regulated and abrupt changes in phosphorylation 1 . Mitotic entry is initiated by increased phosphorylation of mitotic proteins, a process driven by kinases 2 , whereas mitotic exit is ac…
View article: Cryo-EM structures of PP2A:B55-FAM122A and PP2A:B55-ARPP19
Cryo-EM structures of PP2A:B55-FAM122A and PP2A:B55-ARPP19 Open
Progression through the cell cycle is controlled by regulated and abrupt changes in phosphorylation. 1 Mitotic entry is initiated by increased phosphorylation of mitotic proteins, a process driven by kinases, 2 while mitotic exit is achiev…
View article: Molecular Mechanism of PP2A/B55α Phosphatase Inhibition by IER5
Molecular Mechanism of PP2A/B55α Phosphatase Inhibition by IER5 Open
PP2A serine/threonine phosphatases are heterotrimeric complexes that execute many essential physiologic functions. These activities are modulated by additional regulatory proteins, such as ARPP19, FAM122A, and IER5. Here, we report the cry…
View article: Supplementary Methods and Figures S1-S4 from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase
Supplementary Methods and Figures S1-S4 from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase Open
Supplementary Methods Supplementary References Figure S1. PIM and PI3K/AKT inhibitors synergize to suppress PCa cell growth and survival. Figure S2. PIM1 induces expression of ROS scavengers by NRF2 transcription activity. Figure S3. PIM1 …
View article: Data from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Data from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Despite significant progress in understanding the genetic landscape of T-cell acute lymphoblastic leukemia (T-ALL), the discovery of novel therapeutic targets has been difficult. Our results demonstrate that the levels of PIM1 protein kina…
View article: Data from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase
Data from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase Open
Cancer resistance to PI3K inhibitor therapy can be in part mediated by increases in the PIM1 kinase. However, the exact mechanism by which PIM kinase promotes tumor cell resistance is unknown. Our study unveils the pivotal control of redox…
View article: Supplementary Methods and Figures S1-S4 from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase
Supplementary Methods and Figures S1-S4 from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase Open
Supplementary Methods Supplementary References Figure S1. PIM and PI3K/AKT inhibitors synergize to suppress PCa cell growth and survival. Figure S2. PIM1 induces expression of ROS scavengers by NRF2 transcription activity. Figure S3. PIM1 …
View article: Table S4-5 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S4-5 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S4: GSEA curated canonical pathway enrichment (FDR<0.25) Table S5: GSEA oncogenic signature enrichment of AZDR1 compared to Naïve HSB-2 (FDR<0.25)
View article: Table S11-14 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S11-14 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S11: RPPA differential abundance in AZD1208 resistant compared to DMSO treated HSB-2 cells. Table S12: RPPA differential abundance in AZD-1µM (AZD1208 sensitive) compared to AZDR1 HSB-2 cells. Table S13: RPPA differential abundance i…
View article: Data from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase
Data from Mechanisms Behind Resistance to PI3K Inhibitor Treatment Induced by the PIM Kinase Open
Cancer resistance to PI3K inhibitor therapy can be in part mediated by increases in the PIM1 kinase. However, the exact mechanism by which PIM kinase promotes tumor cell resistance is unknown. Our study unveils the pivotal control of redox…
View article: Table S6-10 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S6-10 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S6:Functional enrichment of KEGG pathways in RNA-seq active module. Table S7: Testing for protein-protein interaction network bias in active module analysis with KEGG pathway functional enrichment (Trial 1). Table S8: Testing for pro…
View article: Table S11-14 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S11-14 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S11: RPPA differential abundance in AZD1208 resistant compared to DMSO treated HSB-2 cells. Table S12: RPPA differential abundance in AZD-1µM (AZD1208 sensitive) compared to AZDR1 HSB-2 cells. Table S13: RPPA differential abundance i…
View article: Supplementary Appendix file from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Supplementary Appendix file from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Supplementary Materials and Methods, Tables and References
View article: Table S4-5 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S4-5 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S4: GSEA curated canonical pathway enrichment (FDR<0.25) Table S5: GSEA oncogenic signature enrichment of AZDR1 compared to Naïve HSB-2 (FDR<0.25)
View article: Supplementary Appendix file from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Supplementary Appendix file from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Supplementary Materials and Methods, Tables and References
View article: Table S2-3 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S2-3 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S2: GO terms enriched from hierarchical clustering with optimal cut tree on differentially expressed (FDR<0.01) genes in AZDR1 compared to Naïve HSB-2. Table S3: GO terms enriched from hierarchical clustering with cut tree at h=2 on …
View article: Data from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Data from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Despite significant progress in understanding the genetic landscape of T-cell acute lymphoblastic leukemia (T-ALL), the discovery of novel therapeutic targets has been difficult. Our results demonstrate that the levels of PIM1 protein kina…
View article: Table S2-3 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S2-3 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S2: GO terms enriched from hierarchical clustering with optimal cut tree on differentially expressed (FDR<0.01) genes in AZDR1 compared to Naïve HSB-2. Table S3: GO terms enriched from hierarchical clustering with cut tree at h=2 on …
View article: Table S6-10 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
Table S6-10 from PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Table S6:Functional enrichment of KEGG pathways in RNA-seq active module. Table S7: Testing for protein-protein interaction network bias in active module analysis with KEGG pathway functional enrichment (Trial 1). Table S8: Testing for pro…
View article: Table2_KDs_FAM122A_Compiled.xlsx
Table2_KDs_FAM122A_Compiled.xlsx Open
Data for activity and binding
View article: ARPP19_FAM122A_data
ARPP19_FAM122A_data Open
Data for supporting manuscript
View article: “Root”ing for successful T-ALL treatment
“Root”ing for successful T-ALL treatment Open
In this issue of Blood, Anand et al(1) provide compelling evidence that resistance to Notch inhibitor therapy in early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) occurs as a result of an activated phosphatidylinositol 3-kinase…
View article: PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis
PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis Open
Despite significant progress in understanding the genetic landscape of T-cell acute lymphoblastic leukemia (T-ALL), the discovery of novel therapeutic targets has been difficult. Our results demonstrate that the levels of PIM1 protein kina…
View article: PIM protein kinases regulate the level of the long noncoding RNA H19 to control stem cell gene transcription and modulate tumor growth
PIM protein kinases regulate the level of the long noncoding RNA H19 to control stem cell gene transcription and modulate tumor growth Open
The proviral integration site for Moloney murine leukemia virus (PIM) serine/threonine kinases have an oncogenic and prosurvival role in hematological and solid cancers. However, the mechanism by which these kinases drive tumor growth has …
View article: Phosphorylation of DEPDC5, a component of the GATOR1 complex, releases inhibition of mTORC1 and promotes tumor growth
Phosphorylation of DEPDC5, a component of the GATOR1 complex, releases inhibition of mTORC1 and promotes tumor growth Open
Significance The mTORC1 (mammalian target of rapamycin complex 1) pathway plays a critical role in driving cancer growth. We have identified a phosphorylation-dependent mechanism that controls mTORC1 activity in which Pim and AKT kinases, …