|1.||Shuin, Taro: 4 articles (11/2007 - 08/2004)|
|2.||Okuda, Heiwa: 3 articles (11/2007 - 06/2005)|
|3.||Ahn, Dae-Ro: 2 articles (03/2013 - 08/2009)|
|4.||Conaway, Ronald C: 2 articles (03/2008 - 02/2005)|
|5.||Conaway, Joan W: 2 articles (03/2008 - 02/2005)|
|6.||Aso, Teijiro: 2 articles (11/2007 - 01/2007)|
|7.||Ashida, Shingo: 2 articles (06/2006 - 08/2004)|
|8.||Tamura, Kenji: 2 articles (06/2006 - 08/2004)|
|9.||Deng, Yuqing: 1 article (10/2015)|
|10.||Yang, Yongqing: 1 article (10/2015)|
04/01/2014 - "A large majority of tumors (33/43) showed very low to undetectable Elongin A3 expression and as expected 89% (40/45) displayed one gene copy of TCEB3C. "
06/01/2005 - "Moreover, a mutation in the elongin-binding domain may induce type 2B tumors through different molecular pathways compared to those induced by type 1- or 2A-associated mutations in the HIF-alpha -binding region."
05/01/2003 - "Here we use the yeast Saccharomyces cerevisiae as a model system to examine in vivo the chaperone requirements for assembly of the von Hippel-Lindau protein (VHL)-elongin BC (VBC) tumor suppressor complex. "
07/18/2000 - "Because the elongin-binding domain of VHL is frequently mutated in cancers, these results suggest that loss of elongin binding causes tumorigenesis by compromising VHL protein stability and/or potential VHL ubiquitination functions."
07/18/2000 - "A preponderance of the tumor-disposing inherited missense mutations detected in VHL disease are within the elongin-binding domain of VHL. "
06/08/2007 - "Using hypoxia-inducible factor-1alpha (HIF-1alpha), a substrate of the Elongin B/C-Cul2-VHL ligase, we demonstrate the critical role of substrate binding to promote Cul2 neddylation in a manner that does not require substrate ubiquitination but may involve a conformational change. "
06/01/2005 - "These occur in the pVHL regions that bind hypoxia-inducible factor alpha (HIF-alpha ) or Elongin C. "
02/01/1998 - "A model for the regulation of hypoxia-inducible mRNAs by pVHL is presented based on the apparent similarity of elongin C and Cul2 to Skp1 and Cdc53, respectively. "
02/01/1998 - "pVHL mutants that were unable to bind to complexes containing elongin C and Cul2 were likewise unable to inhibit the accumulation of hypoxia-inducible mRNAs. "
06/01/2006 - "Inactivation of the VHL tumor suppressor protein with loss of function of the VHL protein, and Elongin B, C complex results in a dysfunction of the ubquitination of hypoxia-inducible factor, which is an important step in the development of highly vascular tumors. "
|3.||Renal Cell Carcinoma (Grawitz Tumor)
03/24/2000 - "They also suggest that sequences outside the elongin C binding box may function as a nuclear export domain, potentially providing a novel role for this region of VHL frequently mutated in renal cell carcinoma."
09/25/1998 - "Naturally occurring pVHL mutants which fail to interact with elongin have been described in patients with VHL disease or sporadic renal cell carcinoma (RCC). "
11/24/2005 - "Role of elongin-binding domain of von Hippel Lindau gene product on HuR-mediated VPF/VEGF mRNA stability in renal cell carcinoma."
08/16/2001 - "The pVHL-associated SCF ubiquitin ligase complex: molecular genetic analysis of elongin B and C, Rbx1 and HIF-1alpha in renal cell carcinoma."
12/01/1997 - "Patients with von Hippel-Lindau (VHL) syndrome develop renal cell carcinoma and it has been shown that VHL protein inhibits elongin, a cellular transcription factor which controls RNA elongation. "
03/05/1996 - "The product of the von Hippel-Lindau (VHL) tumor suppressor gene, the gene inactivated in VHL disease and in sporadic clear-cell renal carcinomas, has recently been shown to have as a functional target the transcription elongation complex, elongin (also called SIII). "
05/01/2002 - "Here, fluorescence in situ hybridization on tissue microarray showed high-level amplification of the Elongin C gene in 8 (23%) of 35 hormone-refractory carcinomas but in none of the untreated prostate carcinomas (n = 35). "
12/01/2010 - "Epigenetic silencing by promoter DNA methylation for VHL and the complex genes, CUL2, elongin C (TCEB1), elongin B (TCEB2) and RBX1, is unlikely to play a role in HIF-1α upregulation in breast carcinomas."
09/29/1998 - "pVHL19, like pVHL30, can bind to elongin B, elongin C, and Hs-Cul2 in coimmunoprecipitation assays and can inhibit the production of hypoxia-inducible proteins such as vascular endothelial growth factor (VEGF) and GLUT1 when reintroduced into renal carcinoma cells that lack a wild-type VHL allele. "
11/17/2009 - "The recruitment of p300 and pol II rapidly transitions to the assembly of several elongation factors, including the positive transcriptional elongation factor (P-TEFb), the bromodomain-containing protein (BRD4), and the elongin-like eleven nineteen lysine-rich leukemia protein (ELL). "
06/01/2002 - "ELL (Eleven-nineteen Lysine rich Leukemia) is known to be an elongation factor resembling elongin for RNA polymerase II transcription. "
01/01/1999 - "Among these candidate general elongation factors are the positive transcription elongation factor b (P-TEFb), eleven-nineteen lysine-rich in leukemia (ELL), Cockayne syndrome complementation group B (CSB), and elongin proteins, which all function in vitro to expedite elongation by RNA polymerase II by suppressing transient pausing or premature arrest by polymerase through direct interactions with the elongation complex. "
|3.||RNA Polymerase II (RNA Polymerase B)
|4.||Peptide Elongation Factors (Elongation Factor)
|5.||Ubiquitin-Protein Ligases (Ubiquitin-Protein Ligase)
|6.||Proteins (Proteins, Gene)
|7.||DNA Polymerase II
|8.||Von Hippel-Lindau Tumor Suppressor Protein
|9.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)