Smad6 and uses thereof
AssigneeJapanese Foundation for Cancer Research
InventorsKohei Miyazono, Masahiro Kawabata
Life of this patent
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Abstract
The invention describes nucleic acids encoding the Smad6 protein, including fragments and biologically functional variants thereof. Also included are polypeptides and fragments thereof encoded by such nucleic acids, and antibodies relating thereto. Methods and products for using such nucleic acids and polypeptides also are provided.
Claims15
An isolated nucleic acid molecule selected from the group consisting of
- (a) nucleic acid molecules which hybridize under stringent conditions to a molecule consisting of the nucleic acid sequence of SEQ ID NO:1 and which code for a polypeptide which inhibits TGF-β superfamily signalling, provided that the nucleic acid molecules exclude sequences consisting only of SEQ ID NO:4, wherein the stringent conditions are selected from the group consisting of (1) hybridization at 65° C. in hybridization buffer (3.5×SSC, 0.02% Ficoll, 0.02% polyvinyl pyrrolidone, 0.02% Bovine Serum Albumin, 2.5 mM NaH2PO4(pH7), 0.5% SDS, 2 mM EDTA), wherein SSC is 0.15M sodium chloride/0.15M sodium citrate, pH7, SDS is sodium dodecyl sulphate, and EDTA is ethylenediaminetetracetic acid;
- and (2) hybridization at 65° C. in 5×SSC, 1% SDS, 5×Denhardt's solution and 10 μg/ml salmon sperm DNA,
- (b) nucleic acid molecules that differ from the nucleic acid molecules of (a) in codon sequence due to the degeneracy of the genetic code, and
- (c) complements of (a) and (b).
An isolated nucleic acid molecule selected from the group consisting of (a) a functional fragment of SEQ ID NO:3 between 20 and 1487 nucleotides in length, and (b) complements of “(a)”, provided that the nucleic acid molecule includes a portion of SEQ ID NO:3 which is not overlapped by SEQ ID NO:4, wherein the functional fragment has a function selected from the group consisting of inhibition of TβR-I signaling, inhibition of ActR-I signaling, inhibition of BMPR-IB signaling, inhibition of Smad1 phosphorylation, inhibition of Smad2 phosphorylation, binding to TβR-I, binding to ActR-I and binding to BMPR-IB.
Dependencies are inferred from the claim text.