Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
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 Kits (7) und Cbl Proto-Oncogene B, E3 Ubiquitin Protein Ligase Proteine (5) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 78 products:
MMAB (zeige MMAB Antikörper) 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 Antikörper), 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 Antikörper) is the most likely gene influencing high-density lipoprotein-cholesterol levels at MMAB (zeige MMAB Antikörper)-MVK (zeige MVK Antikörper) locus.
Characterization of ligand-binding by MMAB (zeige MMAB Antikörper) 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 Antikörper) that are found in normal individuals, and their interactions with methionine synthase reductase (zeige MTRR Antikörper).
Mutations in methylmalonic aciduria type B protein (zeige MMAB Antikörper) 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 Antikörper) and CBL-B in epithelial stem cell maintenance during organ development and remodeling through modulation of mTOR (zeige FRAP1 Antikörper) signaling.
CBLB directs polyubiquitination of dectin-1 (zeige CLEC7A Antikörper) and dectin-2 (zeige CLEC6A Antikörper), two key pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK (zeige SYK Antikörper), thus inhibiting dectin-1 (zeige CLEC7A Antikörper)- and dectin-2 (zeige CLEC6A Antikörper)-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 Antikörper)-mediated antifungal innate immunity
Fasudil, a clinically safe ROCK inhibitor, decreases disease burden in a Cbl/Cbl (zeige CBL Antikörper)-b deficiency-driven murine model of myeloproliferative disorders.
Mechanistically, NFATc1 (zeige NFATC1 Antikörper) induces Nur77 (zeige NR4A1 Antikörper) expression at late stage of osteoclast differentiation; in turn, Nur77 (zeige NR4A1 Antikörper) transcriptionally up-regulates E3 ubiquitin ligase (zeige MUL1 Antikörper) Cbl-b, which triggers NFATc1 (zeige NFATC1 Antikörper) 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