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Negatively regulates endocytic trafficking. Additionally we are shipping KIAA0226 Proteins (2) and and many more products for this protein.
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Rubicon thus functions as an important negative regulator of the innate immune response, enhances viral replication and may play a role in viral immune evasion.
HCV, by differentially inducing the expression of Rubicon and UVRAG (show UVRAG Antibodies), temporally regulated the autophagic flux to enhance its replication.
This study demonistrated that KIAA0226 mutation impairs Rubicon endosomal localization
New DNA sequencing technologies are enabling us to investigate the whole or large targeted proportions of the genome in a rapid, affordable, and comprehensive way. Exome and targeted sequencing rundataxin genes causing ataxia.
Rubicon may thus be pivotal to generating an optimal intracellular immune response against microbial infection.
Rubicon differentially targets signaling complexes, depending on environmental stimuli, and may function to coordinate various immune responses against microbial infection.
Rubicon and PLEKHM1 (show PLEKHM1 Antibodies) specifically and directly interact with Rab7 (show RAB7B Antibodies) via their RH domain; this interaction is critical for their function; show Rubicon but not PLEKHM1 (show PLEKHM1 Antibodies) uniquely regulates membrane trafficking via simultaneously binding both Rab7 (show RAB7B Antibodies) and PI3-kinase (show PIK3CA Antibodies)
a critical role of the Rubicon RUN domain in PI3KC3 and autophagy regulation
Rubicon serves as a previously unknown Rab7 (show RAB7B Antibodies) effector to ensure the proper progression of the endocytic pathway.
we report the identification of a family with three children affected with a new form of recessive ataxia, which we suggest naming 'Salih ataxia', and of a frameshift mutation of KIAA0226 (rundataxin) that segregates with the disease
Rubicon specifically interacts with the interferon regulatory factor (IRF) association domain (IAD) of IRF3, and this interaction leads to inhibition of the dimerization of IRF3, which negatively regulates interferon-mediated antiviral response.
Rubicon deficiency enhances autophagic flux in the heart and protects mice from lethality and reduction in stroke volume induced by LPS (show TLR4 Antibodies).
Data indicate that Rubicon (Kiaa0226) and NOX2 (gp91phox (show CYBB Antibodies)) are involved in microtubule-associated protein (show SPAG5 Antibodies) LC3 (show MAP1LC3A Antibodies)-associated phagocytosis.
Beclin 1 (show BECN1 Antibodies) and its binding proteins orchestrate the precise function of the class III PI(3 (show PI3 Antibodies))K in regulating autophagy at multiple steps.
Two Beclin 1 (show BECN1 Antibodies) associated proteins, Atg14L and Rubicon, were identified.
Negatively regulates endocytic trafficking. Impairs the autophagosome maturation process. May inhibit PIK3C3 activity.
, RUN domain and cysteine-rich domain containing, Beclin 1-interacting protein
, RUN domain protein as Beclin 1-interacting and cysteine-rich containing
, beclin-1 associated RUN domain containing protein
, run domain Beclin-1 interacting and cystein-rich containing protein
, run domain Beclin-1 interacting and cysteine-rich containing protein