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SMAD2 (SMAD family member 2) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and an approved or late-stage drug is recorded against it. Tied to Colorectal cancer, Skin cancer, Gastric & gastro-oesophageal junction cancer and 1 more.
Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD2/SMAD4 complex, activates transcription. Promotes TGFB1-mediated transcription of odontoblastic differentiation genes in dental papilla cells.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.80 (direct and indirect evidence; datatypes literature 0.98, affected pathway 0.76, genetic association 0.59, somatic mutation 0.94). IntOGen calls it a driver in 5 cohorts (2 activating, 3 loss-of-function), covering Colon Adenocarcinoma, Colorectal Adenocarcinoma. In OnCo, 1 product record names it (Luspatercept).
In plain words · SMAD2 (SMAD family member 2) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and an approved or late-stage drug is recorded against it. Tied to Colorectal cancer, Skin cancer, Gastric & gastro-oesophageal junction cancer and 1 more.
SMAD2 (SMAD family member 2) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and an approved or late-stage drug is recorded against it. Tied to Colorectal cancer, Skin cancer, Gastric & gastro-oesophageal junction cancer and 1 more.
Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases.
No product in this corpus aims at SMAD2 yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
Tumour-specific alteration: 1 of 1 medicines aimed at it name a mutant, fusion, exon or hotspot in their mechanism (Luspatercept), an alteration absent from normal cells. HPA SMAD2: RNA low tissue specificity; high antibody staining in 11 normal tissues; highest cancer staining colorectal cancer (4 of 12 high). Distribution: 3 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Colorectal cancer, Skin cancer (all types), Gastric & gastro-oesophageal junction cancer); Open Targets associates it with 1 specific cancer type at or above 0.5 (colorectal adenocarcinoma). (Rule 4 of scripts/fetch-target-specificity.ts.)
Sources: COMMANDS (Lancet 2023); Human Protein Atlas SMAD2 tissue; Open Targets ENSG00000175387 associations
First described 1996. Earliest sequence paper UniProt cites for the protein: Riggins G.J. et al, Nat. Genet, 1996, "Mad-related genes in the human". Source.
Sources: HGNC HGNC:6768 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q15796 (protein name, function text, keywords and locations (REST API)); CIViC gene SMAD2 (1 evidence items, 0 assertions, 1 variants; diseases: (GraphQL API, CC0)); Open Targets ENSG00000175387 (association with cancer (MONDO_0004992) 0.80; per-cancer scores at or above 0.5: colorectal cancer 0.67, gastric cancer 0.52, melanoma 0.55, skin cancer 0.54 (GraphQL API, CC0)); IntOGen SMAD2 (driver in 5 cohorts (Act 2, LoF 3); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD2/SMAD4 complex, activates transcription. Promotes TGFB1-mediated transcription of odontoblastic differentiation genes in dental papilla cells. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator. May act as a tumour suppressor in colorectal carcinoma. Location: Cytoplasm; Nucleus (UniProt). Locus 18q21.1 (HGNC).
RNA: low tissue specificity, detected in all normal tissues.
Medium: Adipose tissue, Adrenal gland, Appendix, Bone marrow, Bronchus, Caudate, Cervix, Duodenum.
Medium only: breast cancer, carcinoid, cervical cancer, glioma.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Query for this target: (TITLE:"SMAD2" OR ABSTRACT:"SMAD2" OR TITLE:"SMAD family member 2" OR ABSTRACT:"SMAD family member 2" OR TITLE:"MADR2" OR ABSTRACT:"MADR2" OR TITLE:"JV18-1" OR ABSTRACT:"JV18-1" OR TITLE:"MADH2" OR ABSTRACT:"MADH2") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about SMAD2, not a curated reading list.
Shares TGF-β signalling, IntOGen, Gastric & gastro-oesophageal junction cancer, Open Targets Platform.
Shares TGF-β signalling, IntOGen, Open Targets Platform.
Shares TGF-β signalling, IntOGen, Gastric & gastro-oesophageal junction cancer, Open Targets Platform.
Shares TGF-β signalling, Open Targets Platform, Colorectal cancer.
Shares Luspatercept, TGF-β signalling.
Shares TGF-β signalling, Colorectal cancer.
Shares TGF-β signalling, Colorectal cancer.
Shares TGF-β signalling, Colorectal cancer.