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抗Human Mahogunin RING Finger Protein 1 抗体:
抗Mouse (Murine) Mahogunin RING Finger Protein 1 抗体:
抗Rat (Rattus) Mahogunin RING Finger Protein 1 抗体:
Regulation of Mfn1 (显示 MFN1 抗体) by MGRN1 and the proteasome modulates mitochondrial fusion.
With aging, the neuroprotective e3 ligase MGRN1 relocates from the cytosol to the nucleus of neurons, where it associates with chromatin and potentiates the cellular response to proteotoxic stress. This nuclear shift is due to a proteasome impairment dependent increase of a monoubiquitinated form of MGRN1.
Catalytic inactivation of MGRN1 results in elevated levels of GP78 (显示 AMFR 抗体) and a consequential increase in the initiation of mitophagy.
Mahogunin-mediated alpha-tubulin (显示 TUBA4A 抗体) ubiquitination via noncanonical K6 linkage regulates microtubule stability and mitotic spindle orientation.
data suggest that MGRN1 selectively targets misfolded proteins for degradation and may exhibit viable therapeutic potential for the treatment of spongiform neurodegeneration
It therefore seems probable that the role of MGRN1 in the adrenal relates to the trafficking and/or degradation of the melanocortin 2 receptor (显示 MC2R 抗体).
a role for Mahogunin in a proteasome-independent ubiquitylation pathway: TSG101 (显示 TSG101 抗体) is a specific Mahogunin substrate
Study shows that both (Ctm)PrP and cyPrP can interact with and disrupt the function of Mahogunin (Mgrn), a cytosolic ubiquitin ligase whose loss causes spongiform neurodegeneration.
Findings suggest that mahogunin ring finger-1 contributes to the clearance of toxic mutant copper-zinc superoxide dismutase (显示 SOD1 抗体) inclusions likely through autophagic pathway.
ATRN (显示 ATRN 抗体) also has no effect on prion (显示 PRNP 抗体) disease onset or progression and discuss possible mechanisms that could cause vacuolation of the central nervous system in Mgrn1 and Atrn (显示 ATRN 抗体) null mutant mice
pigment-type switching likely requires MGRN1's ubiquitin ligase activity but not its ability to bind TSG101 or NEDD4.
Levels of the Mahogunin Ring Finger 1 E3 ubiquitin ligase (显示 MUL1 抗体) do not influence prion (显示 PRNP 抗体) disease.
the md and mg mutations rescue the A(y) phenotypes by a primarily cAMP-independent mechanism promoting trafficking of MC4R (显示 MC4R 抗体) and likely MC1R (显示 MSHR 抗体) away from the lysosome toward the cell surface.
positional cloning of mahoganoid, encoding a novel 494-amino acid protein containing a C3HC4 RING (really interesting new gene) domain that may function as an E3 ubiquitin ligase (显示 MUL1 抗体)
a null mutation for mahoganoid causes a similar age-dependent neuropathology that includes many features of prion (显示 PRNP 抗体) diseases but without accumulation of protease-resistant prion protein (显示 PRNP 抗体)
Mahoganoid mutation (Mgrn1md) on insulin (显示 INS 抗体) sensitivity suggests that Mgrn1md may be increasing insulin (显示 INS 抗体) sensitivity via the hypothalamic melanocortin-3 receptor (显示 MC3R 抗体) pathway.
Mahogunin (MGRN1) is a C3HC4 RING-containing protein with E3 ubiquitin ligase activity in vitro.
E3 ubiquitin-protein ligase MGRN1
, RING finger protein 156
, mahogunin RING finger protein 1
, mahogunin, ring finger 1
, probable E3 ubiquitin-protein ligase MGRN1
, mahogunin ring finger protein 1