187 Pathways

• Signaling by ERBB2,
• B Cell Activation,
• Innate Immune System,
• G2/M Transition,
• G1 Phase,
• Regulation of Hypoxia-inducible Factor (HIF) by Oxygen,
• Apoptosis,
• p75 NTR receptor-mediated signalling,
• DAP12 interactions,
• Separation of Sister Chromatids,
• Regulation of DNA replication,
• NOTCH2 Activation and Transmission of Signal to the Nucleus,
• Pre-NOTCH Expression and Processing,
• Toll Like Receptor 9 (TLR9) Cascade,
• MyD88 dependent cascade initiated on endosome,
• TGFBR1 KD Mutants in Cancer,
• Loss of Function of SMAD2/3 in Cancer,
• Downregulation of ERBB2:ERBB3 signaling,
• Fc epsilon receptor (FCERI) signaling,
• IRAK2 mediated activation of TAK1 complex,
• Immune System,
• SCF(Skp2)-mediated degradation of p27/p21,
• Regulation of activated PAK-2p34 by proteasome mediated degradation,
• SMAD4 MH2 Domain Mutants in Cancer,
• Mitotic Anaphase,
• p53-Independent G1/S DNA damage checkpoint,
• NOTCH1 Intracellular Domain Regulates Transcription,
• SMAD2/3 MH2 Domain Mutants in Cancer,
• Signaling by Wnt,
• Pre-NOTCH Processing in the Endoplasmic Reticulum,
• Toll Like Receptor 5 (TLR5) Cascade,
• Amplification of signal from the kinetochores,
• Signaling by EGFR in Cancer,
• FBXW7 Mutants and NOTCH1 in Cancer,
• Signaling by FGFR,
• Signaling by NOTCH1,
• Receptor-ligand binding initiates the second proteolytic cleavage of Notch receptor,
• Inactivation of APC/C via direct inhibition of the APC/C complex,
• Cyclin E associated events during G1/S transition,
• Spry regulation of FGF signaling,
• Signaling by NOTCH2,
• Toll-Like Receptors Cascades,
• Autodegradation of Cdh1 by Cdh1:APC/C,
• Constitutive Signaling by NOTCH1 PEST Domain Mutants,
• Signaling by EGFR,
• Beta-catenin phosphorylation cascade,
• Synthesis of DNA,
• Chk1/Chk2(Cds1) mediated inactivation of Cyclin B:Cdk1 complex,
• Mitotic M-M/G1 phases,
• APC/C:Cdc20 mediated degradation of Cyclin B,
• G1/S Transition,
• Orc1 removal from chromatin,
• APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1,
• Double-Strand Break Repair,
• TRIF-mediated TLR3/TLR4 signaling,
• Regulation of PLK1 Activity at G2/M Transition,
• Downstream Signaling Events Of B Cell Receptor (BCR),
• Constitutive Signaling by NOTCH1 HD Domain Mutants,
• Cyclin A/B1 associated events during G2/M transition,
• Downstream signaling of activated FGFR,
• ATM mediated response to DNA double-strand break,
• Signaling by NOTCH1 PEST Domain Mutants in Cancer,
• PI3K events in ERBB4 signaling,
• MyD88 cascade initiated on plasma membrane,
• Signaling by constitutively active EGFR,
• DAP12 signaling,
• Disease,
• SMAD2/3 Phosphorylation Motif Mutants in Cancer,
• Signaling by NOTCH1 in Cancer,
• Activation of NF-kappaB in B Cells,
• Regulation of Apoptosis,
• Class I MHC mediated antigen processing & presentation,
• Loss of Function of SMAD4 in Cancer,
• Loss of Function of TGFBR1 in Cancer,
• Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant,
• Toll Like Receptor TLR1:TLR2 Cascade,
• Downstream signal transduction,
• DNA Repair,
• Signaling by NOTCH,
• Signaling by NGF,
• Switching of origins to a post-replicative state,
• Oxygen-dependent Proline Hydroxylation of Hypoxia-inducible Factor Alpha,
• Signaling by NOTCH1 HD Domain Mutants in Cancer,
• Pre-NOTCH Processing in Golgi,
• Cdc20:Phospho-APC/C mediated degradation of Cyclin A,
• IRAK2 mediated activation of TAK1 complex upon TLR7/8 or 9 stimulation,
• TGFBR2 MSI Frameshift Mutants in Cancer,
• Polo-like kinase mediated events,
• Signaling Pathways,
• Signaling by NOTCH1 HD+PEST Domain Mutants in Cancer,
• Toll Like Receptor 4 (TLR4) Cascade,
• Signaling by SCF-KIT,
• G2/M DNA damage checkpoint,
• Regulation of mitotic cell cycle,
• Signaling by TGF-beta Receptor Complex,
• G2/M Checkpoints,
• Signaling by TGF-beta Receptor Complex in Cancer,
• PI3K/AKT activation,
• Signaling by PDGF,
• MyD88:Mal cascade initiated on plasma membrane,
• Signaling by ERBB4,
• Senescence-Associated Secretory Phenotype (SASP),
• Endosomal Sorting Complex Required For Transport (ESCRT),
• Signaling by NOTCH3,
• SMAD2/SMAD3:SMAD4 heterotrimer regulates transcription,
• Signaling by NODAL,
• PI-3K cascade,
• Homologous recombination repair of replication-independent double-strand breaks,
• Cellular response to hypoxia,
• TGF-beta receptor signaling activates SMADs,
• Transcriptional activity of SMAD2/SMAD3:SMAD4 heterotrimer,
• TRAF6 mediated induction of TAK1 complex,
• Role of LAT2/NTAL/LAB on calcium mobilization,
• Circadian Clock,
• Antigen processing: Ubiquitination & Proteasome degradation,
• Cross-presentation of soluble exogenous antigens (endosomes),
• Mitotic Metaphase and Anaphase,
• Regulation of APC/C activators between G1/S and early anaphase,
• APC/C:Cdc20 mediated degradation of Securin,
• NGF signalling via TRKA from the plasma membrane,
• Cyclin A:Cdk2-associated events at S phase entry,
• Homologous Recombination Repair,
• G1/S DNA Damage Checkpoints,
• Constitutive Signaling by NOTCH1 t(7;9)(NOTCH1:M1580_K2555) Translocation Mutant,
• PI3K events in ERBB2 signaling,
• SCF-beta-TrCP mediated degradation of Emi1,
• Mitotic G1-G1/S phases,
• Signaling by FGFR in disease,
• APC-Cdc20 mediated degradation of Nek2A,
• Generic Transcription Pathway,
• p53-Independent DNA Damage Response,
• S Phase,
• Downregulation of ERBB4 signaling,
• Toll Like Receptor 7/8 (TLR7/8) Cascade,
• Signaling by Activin,
• p75NTR signals via NF-kB,
• Cell Cycle Checkpoints,
• Removal of licensing factors from origins,
• M/G1 Transition,
• Cellular responses to stress,
• MyD88-independent cascade,
• Activated NOTCH1 Transmits Signal to the Nucleus,
• TGFBR2 Kinase Domain Mutants in Cancer,
• TRAF6 mediated induction of NFkB and MAP kinases upon TLR7/8 or 9 activation,
• Toll Like Receptor 3 (TLR3) Cascade,
• CDK-mediated phosphorylation and removal of Cdc6,
• APC/C-mediated degradation of cell cycle proteins,
• Cellular Senescence,
• NF-kB is activated and signals survival,
• PI3K/AKT Signaling in Cancer,
• M Phase,
• Toll Like Receptor 2 (TLR2) Cascade,
• TRAF6 Mediated Induction of proinflammatory cytokines,
• Gene Expression,
• Inhibition of the proteolytic activity of APC/C required for the onset of anaphase by mitotic spindle checkpoint components,
• Loss of Function of TGFBR2 in Cancer,
• Developmental Biology,
• Cell Cycle,
• Toll Like Receptor TLR6:TLR2 Cascade,
• Signaling by NOTCH4,
• Fanconi Anemia pathway,
• Adaptive Immune System,
• Mitotic G2-G2/M phases,
• Toll Like Receptor 10 (TLR10) Cascade,
• G2/M DNA replication checkpoint,
• DNA Replication,
• DNA Replication Pre-Initiation,
• Cyclin D associated events in G1,
• Antigen processing-Cross presentation,
• Activated TLR4 signalling,
• Cell Cycle, Mitotic,
• Membrane Trafficking,
• Amplification of signal from unattached kinetochores via a MAD2 inhibitory signal,
• Conversion from APC/C:Cdc20 to APC/C:Cdh1 in late anaphase,
• Negative regulation of FGFR signaling,
• APC/C:Cdc20 mediated degradation of mitotic proteins,
• TGFBR1 LBD Mutants in Cancer,
• Downregulation of SMAD2/3:SMAD4 transcriptional activity,
• Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants,
• Degradation of beta-catenin by the destruction complex,
• Downregulation of TGF-beta receptor signaling,
• EGFR downregulation,
• Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins,
• Ubiquitin Mediated Degradation of Phosphorylated Cdc25A,
• ER-Phagosome pathway,
• Mitotic Spindle Checkpoint,
• GAB1 signalosome