SAMD4B, a novel SAM-containing protein, inhibits AP-1-, p53- and p21-mediated transcriptional activity

BMB Rep. 2010 May;43(5):355-61. doi: 10.5483/bmbrep.2010.43.5.355.

Abstract

The sterile alpha motif (SAM) is a putative protein interaction domain involved in a wide variety of biological processes. Here we report the identification and characterization of a novel gene, SAMD4B, which encodes a putative protein of 694 amino acids with a SAM domain. Northern blot and RT-PCR analysis showed that SAMD4B is widely expressed in human embryonic and adult tissues. Transcriptional activity assays show SAMD4B suppresses transcriptional activity of L8G5-luciferase. Over-expression of SAMD4B in mammalian cells inhibited the transcriptional activities of activator protein-1 (AP-1), p53 and p21, and the inhibitory effects can be relieved by siRNA. Deletion analysis indicates that the SAM domain is the main region for transcriptional suppression. The results suggest that SAMD4B is a widely expressed gene involved in AP-1-, p53-and p21-mediated transcriptional signaling activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Cell Line
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism*
  • Embryo, Mammalian / anatomy & histology
  • Embryo, Mammalian / metabolism
  • Evolution, Molecular
  • Female
  • Humans
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism*
  • RNA Interference
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism*
  • Signal Transduction
  • Tissue Distribution
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / metabolism*
  • Transcription, Genetic*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Cyclin-Dependent Kinase Inhibitor p21
  • Protein Isoforms
  • Repressor Proteins
  • SAMD4A protein, human
  • SAMD4B protein, human
  • Transcription Factor AP-1
  • Tumor Suppressor Protein p53
  • JNK Mitogen-Activated Protein Kinases