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Ubiquitin-like modifier activating enzyme 7

UBE1L, D-8, Ube-2
The modification of proteins with ubiquitin is an important cellular mechanism for targeting abnormal or short-lived proteins for degradation. Ubiquitination involves at least three classes of enzymes: ubiquitin-activating enzymes, or E1s, ubiquitin-conjugating enzymes, or E2s, and ubiquitin-protein ligases, or E3s. This gene encodes a member of the E1 ubiquitin-activating enzyme family. The encoded enzyme is a retinoid target that triggers promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARalpha) degradation and apoptosis in acute promyelocytic leukemia, where it is involved in the conjugation of the ubiquitin-like interferon-stimulated gene 15 protein. [provided by RefSeq, Jul 2008] (from NCBI)
Papers on UBE1L
The defective nuclear lamina in Hutchinson-gilford progeria syndrome disrupts the nucleocytoplasmic Ran gradient and inhibits nuclear localization of Ubc9.
Paschal et al., Charlottesville, United States. In Mol Cell Biol, 2011
the cellular effects of progerin expression in Hutchinson-Gilford progeria syndrome are transduced, at least in part, through reduced function of the Ran GTPase and E2 SUMOylation pathways.
Hematopoietic cells from Ube1L-deficient mice exhibit an impaired proliferation defect under the stress of bone marrow transplantation.
Zhang et al., San Diego, United States. In Blood Cells Mol Dis, 2010
Bone marrow transplantation experiment revealed a 50% reduction in repopulation potential of Ube1L-deficient cells at 3weeks posttransplantation, but no differences at 6 and 12weeks.
ISG15 Arg151 and the ISG15-conjugating enzyme UbE1L are important for innate immune control of Sindbis virus.
Virgin et al., Saint Louis, United States. In J Virol, 2009
The importance of UbE1L was confirmed by demonstrating that mice lacking this ISG15 E1 enzyme were highly susceptible to Sindbis virus infection.
Mice lacking the ISG15 E1 enzyme UbE1L demonstrate increased susceptibility to both mouse-adapted and non-mouse-adapted influenza B virus infection.
Lenschow et al., Saint Louis, United States. In J Virol, 2009
Both UbE1L(-/-) and ISG15(-/-) mice display increased susceptibility to influenza B virus infection, including non-mouse-adapted strains.
UBE1L causes lung cancer growth suppression by targeting cyclin D1.
Dmitrovsky et al., United States. In Mol Cancer Ther, 2008
UBE1L-ISG15 preferentially inhibits cyclin D1 in lung cancer
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