EC Number   |
General Information |
Reference |
|---|
   2.3.2.26 | malfunction |
enzyme knockdown in C2C12 myotubes results in a concurrent increase in Sox6 protein levels and a decrease of Myh7 transcription |
737267 |
| 2.3.2.26 | malfunction |
enzyme knockdown inhibits thioredoxin-interacting protein degradation and results in a subsequent increase in cardiomyocyte apoptosis |
736319 |
| 2.3.2.26 | physiological function |
deletion of isoform Rsp5 or mutation of its ligase activity, blocks the nuclear export of mRNAs. Affected messenger RNAs include both total poly(A)+ mRNA and heat-shock mRNAs. Mutation of Rsp5 does not affect nuclear protein import or export. Deletion of RSP5 blocks mRNA export, even under conditions where its essential role in unsaturated fatty acids biosynthesis is bypassed. The ligase activity is required for proper mRNA export |
735318 |
| 2.3.2.26 | physiological function |
depletion of ubiquitin-protein ligase HECTD3 leads to multipolar spindle formation |
690715 |
| 2.3.2.26 | physiological function |
E3 ligase AIP2 positively regulates T-cell activation. Ectopic expression of AIP2 in mouse primary T cells enhances their proliferation and interleukin-2 production by suppressing the apoptosis of T cells. AIP2 interacts with and promotes ubiquitin-mediated degradation of EGR2, a zinc finger transcription factor that has been found to regulate Fas ligand expression during activation-induced T-cell death. Suppression of AIP2 expression by small RNA interference upregulates EGR2, inhibits EGR2 ubiquitination and Fas ligand expression, and enhances the apoptosis of T cells |
705698 |
| 2.3.2.26 | physiological function |
Ehrlichia chaffeensis tandem repeat protein TRP120 is posttranslationally modified by ubiquitin. Ubiquitination occurs through intrinsic and host-mediated HECT ligase activity. HECT E3 ubiquitin ligase, Nedd4L, interacts with TRP120 during infection and also mediates TRP120 ubiquitination. Nedd4L knockdown results in the reduction of TRP120 ubiquitination, decreases ehrlichial infection, and reduces recruitment of TRP120-interacting host protein, PCGF5, to ehrlichial inclusions. TRP120-mediated PCGF5 polyubiquitination is associated with a reduction in PCGF5 levels. Inhibition of ubiquitination with small molecules also significantly decreases ehrlichial infection |
756908 |
| 2.3.2.26 | physiological function |
Ehrlichia chaffeensis tandem repeat protein TRP120 is posttranslationally modified by ubiquitin. Ubiquitination occurs through intrinsic and host-mediated HECT ligase activity. The C-terminal region of TRP120 harbors a functional HECT E3 ligase domain with a conserved catalytic site. TRP120 autoubiquitination occurs in vitro in the presence of host UbcH5b/c E2 enzymes. Human HECT E3 ubiquitin ligase, Nedd4L, interacts with TRP120 during infection and also mediates TRP120 ubiquitination. Nedd4L knockdown results in the reduction of TRP120 ubiquitination, decreases ehrlichial infection, and reduces recruitment of TRP120-interacting host protein, PCGF5, to ehrlichial inclusions. TRP120-mediated PCGF5 polyubiquitination is associated with a reduction in PCGF5 levels. Inhibition of ubiquitination with small molecules also significantly decreases ehrlichial infection |
756908 |
| 2.3.2.26 | physiological function |
HECT E3 ligase adopts an autoinhibited state, in which its multiple WW domains sequester HECT using a multi-lock mechanism. Removing WW2 or WW34 leads to a partial activation of WWP1. The multi-lock regulation mechanism is conserved in WWP2 and Itch, whereas in Nedd4/4 L and Smurf2, a variant version of the multi-lock autoinhibition mode is utilized |
757746 |
| 2.3.2.26 | physiological function |
HECT-E3 ligase ETC-1 is a regulator of the cytoplasmic anaphase inhibitor securin IFY-1 level. RNAi-mediated depletion of ETC-1 stabilizes IFY-1 and cyclin B1 in post-meiosis I embryos. ETC-1 knockdown in a reduced anaphase promoting complex/cyclosome function background causes an embryonic lethal phenotype. In vitro, ETC-1 ubiquitylates IFY-1 and CYB-1 in the presence of the E2 enzyme UBC-18, which functions in pharyngeal development. UBC-18 plays a distinct role together with ETC-1 in regulating the cytoplasmic level of IFY-1 during meiosis |
733701 |
| 2.3.2.26 | physiological function |
HECTD3 depletion can sensitize cancer cells to extrinsic apoptotic stimuli. HECTD3 inhibits TNF-related apoptosis-inducing ligand-induced caspase-8 cleavage in an E3 ligase activity-dependent manner. Mutation of the caspase-8 ubiquitination site at K215 abolishes the HECTD3 protection from TNF-related apoptosis-inducing ligand-induced cleavage |
733626 |
