MUL1
Reactivity: Human, Mouse, Rat
WB, IF (p)
Host: Rabbit
Polyclonal
AbBy Fluor® 750
Application Notes
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-2000,ELISA 1:5000-20000
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
PBS, 50 % glycerol, 0.05 % Proclin 300, 0.05 %BSA
Preservative
ProClin
Precaution of Use
This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
-20 °C
Storage Comment
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Expiry Date
12 months
Target
MUL1
(Mitochondrial E3 Ubiquitin Protein Ligase 1 (MUL1))
Alternative Name
MUL1
Background
Mitochondrial ubiquitin ligase activator of NFKB 1, E3 SUMO-protein ligase MUL1, E3 ubiquitin-protein ligase MUL1, Growth inhibition and death E3 ligase, Mitochondrial-anchored protein ligase, MAPL, Putative NF-kappa-B-activating protein 266, RING finger protein 218, RING-type E3 ubiquitin transferase NFKB 1MUL1 (Mitochondrial E3 Ubiquitin Protein Ligase 1) is a Protein Coding gene. Among its related pathways are Deubiquitination and Metabolism of proteins. Exhibits weak E3 ubiquitin-protein ligase activity. E3 ubiquitin ligases accept ubiquitin from an E2 ubiquitin-conjugating enzyme in the form of a thioester and then directly transfer the ubiquitin to targeted substrates. Can ubiquitinate AKT1 preferentially at Lys-284 involving Lys-48-linked polyubiquitination and seems to be involved in regulation of Akt signaling by targeting phosphorylated Akt to proteosomal degradation. Proposed to preferentially act as a SUMO E3 ligase at physiological concentrations. Plays a role in the control of mitochondrial morphology. Promotes mitochondrial fragmentation and influences mitochondrial localization. The function may implicate its ability to sumoylate DNM1L. Inhibits cell growth. When overexpressed, activates JNK through MAP3K7/TAK1 and induces caspase-dependent apoptosis. Involved in the modulation of innate immune defense against viruses by inhibiting DDX58-dependent antiviral response. Can mediate DDX58 sumoylation and disrupt its polyubiquitination.