Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain. - Wikidata - wikimedia - TriplyDB

Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.

Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.

http://www.wikidata.org/entity/Q40219809

about

FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity Evidence for a genomic mechanism of action for progesterone receptor membrane component-1 Identification of a genetic interaction between the tumor suppressor EAF2 and the retinoblastoma protein (Rb) signaling pathway in C. elegans and prostate cancer cells ELL is an HIF-1alpha partner that regulates and responds to hypoxia response in PC3 cells.NCI60 cancer cell line panel data and RNAi analysis help identify EAF2 as a modulator of simvastatin and lovastatin response in HCT-116 cells.Regulation of fertility, survival, and cuticle collagen function by the Caenorhabditis elegans eaf-1 and ell-1 genes.FOXA1 modulates EAF2 regulation of AR transcriptional activity, cell proliferation, and migration in prostate cancer cells.Dynamic intracellular distribution of Eaf2 and its potential involvement in UV-Induced DNA damage response.Pirin down-regulates the EAF2/U19 protein and alleviates its growth inhibition in prostate cancer cells Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.

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Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.

http://www.wikidata.org/entity/Q40219809

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

Apoptosis induction and growth ...... hrough its ELL-binding domain.

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Apoptosis induction and growth ...... hrough its ELL-binding domain.

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Apoptosis induction and growth ...... hrough its ELL-binding domain.

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Apoptosis induction and growth ...... hrough its ELL-binding domain.

@en

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Federico Simone

http://www.w3.org/2001/XMLSchema#string

Feng Jiang

http://www.w3.org/2001/XMLSchema#string

Junghyun Hahn

http://www.w3.org/2001/XMLSchema#string

Michael J Thirman

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Wuhan Xiao

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Zhou Wang

http://www.w3.org/2001/XMLSchema#string

P2860

CAJAL BODIES: A Long History of Discovery

Cloning of ELL, a gene that fuses to MLL in a t(11;19)(q23;p13.1) in acute myeloid leukemia

ELL binding regulates U19/Eaf2 intracellular localization, stability, and transactivation

An RNA polymerase II elongation factor encoded by the human ELL gene

ELL-associated factors 1 and 2 are positive regulators of RNA polymerase II elongation factor ELL

The elongation domain of ELL is dispensable but its ELL-associated factor 1 interaction domain is essential for MLL-ELL-induced leukemogenesis

Retrovirus-mediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in mice

ELL and EAF1 are Cajal body components that are disrupted in MLL-ELL leukemia

Molecular cloning of human and rat complementary DNA encoding androgen receptors

EAF1, a novel ELL-associated factor that is delocalized by expression of the MLL-ELL fusion protein

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146-153

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scholarly article

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10.1002/PROS.20481

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2

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67

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6751622

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17044034

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2801832

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