Erratum to: hCLP46 increases Smad3 protein stability via inhibiting its ubiquitin-proteasomal degradation

Yingying Xing and Qiaoyun Chu contributed equally to this work. The online version of the original article can be found under doi:10.1007/s13238-015-0174-0.

• Publication year

  2015

• Venue

  Protein & Cell

• Publication date

  2015-07-07

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/s13238-015-0186-9PMID 26150128PMCID 4656208
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• hCLP46 increases Smad3 protein stability via inhibiting its ubiquitin-proteasomal degradation

  2015cited by this paper
• The regulation of TGF-β/SMAD signaling by protein deubiquitination

  2014cited by this paper
• Overexpression of hCLP46 enhances Notch activation and regulates cell proliferation in a cell type‐dependent manner

  2013cited by this paper
• Regulation of mammalian Notch signaling and embryonic development by the protein O-glucosyltransferase Rumi

  2011cited by this paper
• hCLP46 regulates U937 cell proliferation via Notch signaling pathway.

  2011cited by this paper
• Overexpression of Human CAP10-Like Protein 46 KD in T-Acute Lymphoblastic Leukemia and Acute Myelogenous Leukemia

  2010cited by this paper
• Axin and GSK3- control Smad3 protein stability and modulate TGF- signaling.

  2008cited by this paper
• Rumi is a CAP10 domain glycosyltransferase that modifies Notch and is required for Notch signaling.

  2008cited by this paper
• Cloning, expression and characterization of a novel human CAP10-like gene hCLP46 from CD34(+) stem/progenitor cells.

  2006cited by this paper
• CHIP Controls the Sensitivity of Transforming Growth Factor-β Signaling by Modulating the Basal Level of Smad3 through Ubiquitin-mediated Degradation*

  2005cited by this paper
• Contribution of the Constitutive and Inducible Degradation of Smad3 by the Ubiquitin-Proteasome Pathway to Transforming Growth Factor-β Signaling

  2004cited by this paper
• Smad3 potentiates transforming growth factor beta (TGFbeta )-induced apoptosis and expression of the BH3-only protein Bim in WEHI 231 B lymphocytes.

  2003cited by this paper
• Targeted disruption of SMAD3 results in impaired mucosal immunity and diminished T cell responsiveness to TGF‐β

  1999cited by this paper
• Targeted Disruption of Smad3 Reveals an Essential Role in Transforming Growth Factor β-Mediated Signal Transduction

  1999cited by this paper

• No citing papers are available for this paper.