Anti-OTULIN polyclonal antibody (CABT-BL6334)

Specifications


Host Species
Sheep
Antibody Isotype
IgG
Species Reactivity
Human
Immunogen
human OTULIN (residues 1-352)
Conjugate
Unconjugated

Applications


Application Notes
WB: 0.5 µg/ml
IP: Use 0.3 µg/mg of cell extract
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
OTULIN; OTU deubiquitinase with linear linkage specificity; GUM; FAM105B; ubiquitin thioesterase otulin; gumby
Entrez Gene ID
UniProt ID

Citations


Have you cited CABT-BL6334 in a publication? Let us know and earn a reward for your research.

Custom Antibody Labeling


We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

Customer Reviews


Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket

References


Regulation of Met1-linked polyubiquitin signalling by the deubiquitinase OTULIN

FEBS JOURNAL

Authors: Elliott, Paul R.; Komander, David

Modification of proteins with Met1-linked linear' ubiquitin chains has emerged as a key regulatory signal to control inflammatory signalling via the master regulator, the transcription factor nuclear factor B (NF-B). While the assembly machinery, the linear ubiquitin chain assembly complex (LUBAC), and receptors for this ubiquitin chain type have been known for years, it was less clear which deubiquitinating enzymes (DUBs) hydrolyse Met1 linkages specifically. In 2013, two labs reported the previously unannotated protein FAM105B/OTULIN to be this missing Met1 linkage-specific DUB. Structural studies have revealed how OTULIN achieves its remarkable specificity, employing a mechanism of ubiquitin-assisted catalysis in which a glutamate residue on the substrate complements the active site of the enzyme. The specificity of OTULIN enables it to regulate global levels of Met1-linked polyubiquitin in cells. This ability led to investigations of NF-B activation from new angles, and also revealed involvement of Met1-polyubiquitin in Wnt signalling. Interestingly, OTULIN directly interacts with LUBAC, and this interaction is dynamic and can be regulated by OTULIN phosphorylation. This provides a new paradigm for how individual linkage types can be regulated by dedicated enzyme complexes mediating assembly and removal. Here we review what has been learned about OTULIN's mechanism, regulation and function, discuss the open questions in the field, and discuss how DUBs regulate the NF-B response.

Regulation of Linear Ubiquitin Chain Assembly Complex by Caspase-Mediated Cleavage of RNF31

MOLECULAR AND CELLULAR BIOLOGY

Authors: Joo, Donghyun; Tang, Yong; Blonska, Marzenna; Jin, Jianping; Zhao, Xueqiang; Lin, Xin

Cell death and survival signaling pathways have opposed but fundamental functions for various cellular processes and maintain cell homeostasis through cross talk. Here we report a novel mechanism of interaction between these two pathways through the cleavage of RNF31 by caspases. RNF31, a component of the linear ubiquitin chain assembly complex (LUBAC), regulates cell survival by inducing linear ubiquitination of NF-kappa B signaling components. We found that RNF31 is cleaved under apoptosis conditions through various stimulations. The effector caspases caspase 3 and caspase 6 are responsible for this event, and aspartates 348, 387, and 390 were identified as target sites for this cleavage. Cleavage of RNF31 suppressed its ability to activate NF-kappa B signaling; thus, mutation of cleavage sites inhibited the induction of apoptosis by treatment with tumor necrosis factor alpha (TNF-alpha). Our findings elucidate a novel regulatory loop between cell death and the survival signal and may provide guidance for the development of therapeutic strategies for cancers through the sensitization of tumor cells to death-inducing drugs.

Online Inquiry

Name:
Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:

Related Products

Related Resources

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

Inquiry Basket