Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
CBLB encodes a protein that catalyzes the final step in the conversion of vitamin B(12) into adenosylcobalamin (AdoCbl), a vitamin B12-containing coenzyme for methylmalonyl-CoA mutase.
Showing 3 out of 8 products:
analysis of how molecular chaperones interact with ATR in methylmalonic aciduria cblB type
MMAB (Montrer MMAB Kits ELISA) might be a target and potential biomarker of hepatotoxicity in EFV-induced liver toxicity
These findings suggest that rs11066782 in KCTD10, rs11613718 in KCTD10 and rs11067233 in MMAB may contribute to the susceptibility of coronary heart disease by altering plasma HDL-C levels in Han Chinese.
MMAB mutations, including one novel nonsense mutation (c.12 C>A [p.C4X]), were identified in all members of the cblB cohort.
Pathogenicity of the human truncation mutant results from its inability to sequester AdoCbl for direct transfer to methylmalonyl-CoA mutase (Montrer MUT Kits ELISA), resulting in holoenzyme formation.
c.584G>A, c.349-1G>C, and c.290G>A mutations affect the splicing process of ATR.
These data suggest MMAB (Montrer MMAB Kits ELISA) is the most likely gene influencing high-density lipoprotein-cholesterol levels at MMAB (Montrer MMAB Kits ELISA)-MVK (Montrer MVK Kits ELISA) locus.
Characterization of ligand-binding by MMAB (Montrer MMAB Kits ELISA) provides insight into the mechanism of cobalamin adenosylation and the effect of patient mutations in the inherited disorder
report the identification of ATR cDNA as well as the corresponding gene; ATR expression is altered in cell lines derived from cblB methylmalonyl aciduria patients; propose that inborn errors in the ATR gene identified here result in methylmalonyl aciduria
Results describe two common polymorphic variants of ATP:cob(I)alamin adenosyltransferase (Montrer MMAB Kits ELISA) that are found in normal individuals, and their interactions with methionine synthase reductase (Montrer MTRR Kits ELISA).
The establishment of a new model of concurrent tissue-selective CBL/CBL (Montrer CBL Kits ELISA)-B deletion should allow a clear assessment of the tumor-intrinsic roles of CBL/CBL (Montrer CBL Kits ELISA)-B in non-myeloid malignancies and help test the potential for CBL/CBL (Montrer CBL Kits ELISA)-B inactivation in immunotherapy of tumors.
GSK3 catalyzes two previously unreported phosphorylation events at Ser(476) and Ser(480) of Cbl-b. Constitutive activation of PKB in vivo results in a loss of tolerance that is mediated through the downregulation of Cbl-b. The PI3K-PKB-GSK-3 pathway is a novel regulatory axis that is important for controlling the decision between T cell activation and tolerance via Cbl-b.
These studies reveal a novel, cell-autonomous requirement of CBL (Montrer CBL Kits ELISA) and CBL-B in epithelial stem cell maintenance during organ development and remodeling through modulation of mTOR (Montrer FRAP1 Kits ELISA) signaling.
CBLB directs polyubiquitination of dectin-1 (Montrer CLEC7A Kits ELISA) and dectin-2 (Montrer CLEC6A Kits ELISA), two key pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK (Montrer SYK Kits ELISA), thus inhibiting dectin-1 (Montrer CLEC7A Kits ELISA)- and dectin-2 (Montrer CLEC6A Kits ELISA)-mediated innate immune responses.
CBLB controls proximal C-type lectin receptor signaling in macrophages and dendritic cells. CBLB associates with SYK and ubiquitinates SYK, dectin-1, and dectin-2 after fungal recognition. CBLB deficiency results in increased inflammasome activation, enhanced reactive oxygen species production, and increased fungal killing.
study indicates that Cbl-b negatively regulates CLR-mediated antifungal innate immunity
Fasudil, a clinically safe ROCK inhibitor, decreases disease burden in a Cbl/Cbl (Montrer CBL Kits ELISA)-b deficiency-driven murine model of myeloproliferative disorders.
Mechanistically, NFATc1 (Montrer NFATC1 Kits ELISA) induces Nur77 (Montrer NR4A1 Kits ELISA) expression at late stage of osteoclast differentiation; in turn, Nur77 (Montrer NR4A1 Kits ELISA) transcriptionally up-regulates E3 ubiquitin ligase Cbl-b, which triggers NFATc1 (Montrer NFATC1 Kits ELISA) protein degradation.
Silencing Cbl-b significantly enhanced T lymphocyte function and T lymphocyte cytotoxicity activity
mechanisms have therapeutic implications for reducing beta-cell proliferation in insulinomas by inhibiting phospho-HLXB9 or its interaction with Nono and modulating the expression of its direct (Cblb) or indirect (c-Met) targets
This gene encodes a protein that catalyzes the final step in the conversion of vitamin B(12) into adenosylcobalamin (AdoCbl), a vitamin B12-containing coenzyme for methylmalonyl-CoA mutase. Mutations in the gene are the cause of vitamin B12-dependent methylmalonic aciduria linked to the cblB complementation group. Alternatively spliced transcript variants have been found.
, ATP:corrinoid adenosyltransferase
, aquocob(I)alamin vitamin B12s adenosyltransferase
, cob(I)yrinic acid a,c-diamide adenosyltransferase, mitochondrial
, methylmalonic aciduria type B protein
, Casitas B-lineage lymphoma proto-oncogene b
, E3 ubiquitin-protein ligase CBL-B
, RING-type E3 ubiquitin transferase CBL-B
, SH3-binding protein CBL-B
, Signal transduction protein CBL-B
, casitas B-lineage lymphoma proto-oncogene b
, signal transduction protein CBL-B