Reactome: A Curated Pathway Database
Results 1 to 10 of 104
Pathways (26) Reactions (39) Proteins (1) Others (38)
Protein: UniProt:Q13485 SMAD4 (Homo sapiens)
Last changed: 2014-11-25 20:54:06

Pathway: Gene Expression (Homo sapiens)
Gene Expression covers the pathways by which genomic DNA is transcribed to yield RNA, the regulation of these transcription processes, and the pathways by which newly-made RNA Transcripts are processed. Most annotation is centered on the generation of messenger RNAs (mRNAs) by regulated RNA polymerase II (PolII) transcription, although the activities of PolI and PolIII are also covered briefly, as are
Last changed: 2014-11-21 19:49:01

Pathway: Disease (Homo sapiens)
Biological processes are captured in Reactome by identifying the molecules (DNA, RNA, protein, small molecules) involved in them and describing the details of their interactions. From this molecular viewpoint, human disease pathways have three mechanistic causes: the inclusion of microbially-expressed proteins, altered functions of human proteins, or changed expression levels of otherwise functionally
Last changed: 2014-11-21 19:49:01

Pathway: Signal Transduction (Homo sapiens)
Signal transduction is a process in which extracellular signals elicit changes in cell state and activity. Transmembrane receptors sense changes in the cellular environment by binding ligands, such as hormones and growth factors, or reacting to other types of stimuli, such as light. Stimulation of transmembrane receptors leads to their conformational change which propagates the signal to the intracellu
Last changed: 2014-11-21 19:49:01

Pathway: Developmental Biology (Homo sapiens)
As a first step towards capturing the array of processes by which a fertilized egg gives rise to the diverse tissues of the body, examples of three kinds of processes have been annotated. These are aspects of the roles of cell adhesion molecules in axonal guidance and myogenesis, of transcriptional regulation in hematopoiesis (specifically, B lymphopoiesis), pancreatic beta cell and whit
Last changed: 2014-11-21 19:49:01

Pathway: Signaling by BMP (Homo sapiens)
The TGF-beta/BMP (bone morphogenetic protein) pathway incorporates several signalling pathways that share most, but not all, components of a central signal transduction engine. The general signalling scheme is rather simple: upon binding of a ligand, an activated plasma membrane receptor complex is formed, which passes on the signal towards the nucleus through a phosphorylated receptor-activated SMAD (
Last changed: 2014-11-21 14:40:22

Pathway: Generic Transcription Pathway (Homo sapiens)
OVERVIEW OF TRANSCRIPTION REGULATION: Detailed studies of gene transcription regulation in a wide variety of eukaryotic systems has revealed the general principles and mechanisms by which cell- or tissue-specific regulation of differential gene transcription is mediated (reviewed in Naar, 2001. Kadonaga, 2004, Maston, 2006, Barolo, 2002; Roeder, 2005, Rosenfeld, 2006). Of the three maj
Last changed: 2014-11-21 14:40:22

Pathway: SMAD2/3 Phosphorylation Motif Mutants in Cancer (Homo sapiens)
The conserved phosphorylation motif Ser-Ser-X-Ser at the C-terminus of SMAD2 and SMAD3 is subject to disruptive mutations in cancer. The last two serine residues in this conserved motif, namely Ser465 and Ser467 in SMAD2 and Ser423 and Ser425 in SMAD3, are phosphorylated by the activated TGF beta receptor complex (Macias Silva et al. 1996, Nakao et al. 1997). Once phosphorylated, SMAD2 and SMAD3 form t
Last changed: 2014-11-21 14:40:22

Pathway: TGFBR1 KD Mutants in Cancer (Homo sapiens)
Mutations in the kinase domain (KD) of TGF-beta receptor 1 (TGFBR1) have been found in Ferguson-Smith tumor i.e. multiple self-healing squamous epithelioma - MSSE (Goudie et al. 2011), breast cancer (Chen et al. 1998), ovarian cancer (Chen et al. 2001) and head-and-neck cancer (Chen et al. 2001). KD mutations reported in MSSE are nonsense and frameshift mutations that cause premature termination of TGF
Last changed: 2014-11-21 14:40:22

Pathway: SMAD2/3 MH2 Domain Mutants in Cancer (Homo sapiens)
Mutations in the MH2 domain of SMAD2 and SMAD3 affect their ability to form heterotrimers with SMAD4, thereby impairing TGF-beta signaling (Fleming et al. 2013). The SMAD2 and SMAD3 MH2 domain residues most frequently targeted by missense mutations are those that are homologous to SMAD4 MH2 domain residues shown to be involved in the formation of SMAD heterotrimers. Asp300 of SMAD2 and Asp258 of
Last changed: 2014-11-21 14:40:22

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