Elongin

A heterotrimeric protein complex composed of 110 kDa elongin A, 18 kDa elongin B, and 15 kDa elongin C subunits. It functions as a positive regulator of RNA POLYMERASE II, increasing its rate of transcriptional elongation by suppressing transient pausing along the DNA template. Elongin A is the transcriptionally active component; elongins B and C enhance its activity.

Also Known As:

Networked: 71 relevant articles (0 outcomes, 4 trials/studies)

Bio-Agent Context: Research Results

Experts

1.	Shuin, Taro: 4 articles (11/2007 - 08/2004)
2.	Conaway, Joan W: 3 articles (01/2021 - 03/2008)
3.	Conaway, Ronald C: 3 articles (01/2021 - 03/2008)
4.	Aso, Teijiro: 3 articles (01/2017 - 01/2007)
5.	Okuda, Heiwa: 3 articles (11/2007 - 06/2005)
6.	Slaughter, Brian D: 2 articles (01/2021 - 01/2017)
7.	Unruh, Jay R: 2 articles (01/2021 - 01/2017)
8.	Weems, Juston C: 2 articles (01/2021 - 01/2017)
9.	Yasukawa, Takashi: 2 articles (01/2017 - 01/2007)
10.	Ahn, Dae-Ro: 2 articles (03/2013 - 08/2009)

Related Diseases

1.	Neoplasms (Cancer) 01/01/2023 - "The Elongin BC heterodimer (ELOB/C) binds to a BC-box motif and is essential for cancer cell growth. " 01/01/2022 - "Deubiquitylase ovarian tumor domain-containing 6B (OTUD6B) had been documented to couple pVHL and elongin B to form stable VHL - elonginB - elonginC complex, which protects pVHL from degradation. " 01/01/2020 - "Mutations in VHL (von Hippel Lindau) gene, characteristic for this cancer type, lead to altered activity of the trimeric VBC (pVHL-elongin B-C) complex and consequently to HIF-1α stabilization. " 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."
2.	Carcinogenesis 11/14/2022 - "We discovered that DLGAP1-AS2 promoted CRC tumorigenesis and metastasis by physically interacting with Elongin A (ELOA) and inhibiting its protein stability by promoting tripartite motif containing 21 (Trim21)-mediated ubiquitination modification and degradation of ELOA. " 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." 01/01/2014 - "Our results indicate that VHL elongin BC protein complex components other than VHL could be important for PCC tumorigenesis and merit further investigation. " 01/01/2012 - "The Elongin BC complex containing CRL family is now considered two distinct protein assemblies, which play an important role in regulating a variety of cellular processes such as tumorigenesis, signal transduction, cell motility, and differentiation." 08/15/1996 - "PCR analysis of somatic cell hybrids with chromosome 3 translocations and FISH studies utilizing a human YAC clone containing the SII gene further refine the map position of this locus to human chromosome 3p22 --> p21.3. Since another elongation factor, SIII, has been implicated in human carcinogenesis and since the interval within which the human SII gene maps is frequently deleted in certain cancers, elongation factor SII may therefore be considered a candidate gene for human malignancies involving 3p22 --> p21.3."
3.	Cockayne Syndrome (Syndrome, Cockayne) 01/01/2021 - "More recent evidence indicates that the Elongin ubiquitin ligase assembles with the Cockayne syndrome B helicase (CSB) in response to DNA damage and can target stalled polymerases for ubiquitylation and removal from the genome. " 01/01/2021 - "A role for the Cockayne Syndrome B (CSB)-Elongin ubiquitin ligase complex in signal-dependent RNA polymerase II transcription." 01/01/2017 - "Cockayne syndrome B protein regulates recruitment of the Elongin A ubiquitin ligase to sites of DNA damage." 01/01/1999 - "Despite their similar activities in elongation, the P-TEFb, ELL, CSB, and elongin proteins appear to play roles in a diverse collection of human diseases, including human immunodeficiency virus-1 infection, acute myeloid leukemia, Cockayne syndrome, and the familial cancer predisposition syndrome von Hippel-Lindau disease. " 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. "
4.	Melanoma (Melanoma, Malignant) 01/01/2023 - "This study identifies the Elongin BC complex as a key regulator of AXL expression and marker of melanoma differentiation." 01/01/2023 - "Together, the Elongin BC complex regulates AXL and marks a differentiated melanoma phenotype. " 01/01/2023 - "The Elongin BC Complex Negatively Regulates AXL and Marks a Differentiated Phenotype in Melanoma." 01/01/2023 - "RNA-sequencing and IHC analyses of melanoma patient-derived xenografts and clinical samples revealed a negative association between Elongin B/C and dedifferentiation. " 04/01/2000 - "In first-leukapheresis MO, these clones included the following: 1) interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, tumor necrosis factor alpha, growth-related oncogene alpha (GROalpha)/melanoma growth-stimulatory activity, macrophage inflammatory protein 2/GRObeta, ferritin, alpha1-antitrypsin, lysozyme, transaldolase, Epstein-Barr virus-encoded RNA 1 (EBER-1)/EBER-2-associated-protein, thrombospondin 1, an angiotensin receptor II (ATRII) C-terminal homolog, and RNA polymerase II elongation factor (elongin); 2) two clones homologous to functionally undefined genes (BSK-67 and BSK-83); and 3) three unknown cDNA sequences (BSK-66, 80, 89). "
5.	Meningoencephalitis 01/01/2020 - "Our study also shows that the molecular phenotype of LACV NSs is different from RNA polymerase II inhibitors like α-amanitin or Rift Valley fever virus NSs, indicating that LACV is unique in involving the Elongin complex to shut off host transcription and IFN response.IMPORTANCE The mosquito-borne La Crosse virus (LACV; genus Orthobunyavirus, family Peribunyaviridae, order Bunyavirales) is prevalent in the United States and can cause severe childhood meningoencephalitis. "

Related Drugs and Biologics

1.	Amanitins
2.	Proteins (Proteins, Gene)
3.	Ubiquitin
4.	Ligases (Synthetase)
5.	RNA Polymerase II (RNA Polymerase B)
6.	DNA (Deoxyribonucleic Acid)
7.	transcription factor S-II
8.	Elongin
9.	Ubiquitin-Protein Ligases (Ubiquitin-Protein Ligase)
10.	Cullin Proteins (Cullins)

Related Therapies and Procedures

1.	Therapeutics