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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. Zusätzlich bieten wir Ihnen Cbl Proto-Oncogene B, E3 Ubiquitin Protein Ligase Antikörper (78) und Cbl Proto-Oncogene B, E3 Ubiquitin Protein Ligase Proteine (5) und viele weitere Produktgruppen zu diesem Protein an.
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MMAB (zeige MMAB ELISA Kits) 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 (zeige MUT ELISA Kits), 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 (zeige MMAB ELISA Kits) is the most likely gene influencing high-density lipoprotein-cholesterol levels at MMAB (zeige MMAB ELISA Kits)-MVK (zeige MVK ELISA Kits) locus.
Characterization of ligand-binding by MMAB (zeige MMAB ELISA Kits) 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 (zeige MMAB ELISA Kits) that are found in normal individuals, and their interactions with methionine synthase reductase (zeige MTRR ELISA Kits).
Mutations in methylmalonic aciduria type B protein (zeige MMAB ELISA Kits) is associated with methylmalonic acidemia
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 (zeige CBL ELISA Kits) and CBL-B in epithelial stem cell maintenance during organ development and remodeling through modulation of mTOR (zeige FRAP1 ELISA Kits) signaling.
CBLB directs polyubiquitination of dectin-1 (zeige CLEC7A ELISA Kits) and dectin-2 (zeige CLEC6A ELISA Kits), two key pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK (zeige SYK ELISA Kits), thus inhibiting dectin-1 (zeige CLEC7A ELISA Kits)- and dectin-2 (zeige CLEC6A ELISA Kits)-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 (zeige CALCR ELISA Kits)-mediated antifungal innate immunity
Fasudil, a clinically safe ROCK inhibitor, decreases disease burden in a Cbl/Cbl (zeige CBL ELISA Kits)-b deficiency-driven murine model of myeloproliferative disorders.
Mechanistically, NFATc1 (zeige NFATC1 ELISA Kits) induces Nur77 (zeige NR4A1 ELISA Kits) expression at late stage of osteoclast differentiation; in turn, Nur77 (zeige NR4A1 ELISA Kits) transcriptionally up-regulates E3 ubiquitin ligase Cbl-b, which triggers NFATc1 (zeige NFATC1 ELISA Kits) 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
SHP-1 regulates Cbl-b-mediated T cell responses by controlling its tyrosine phosphorylation and ubiquitination
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