GOAT ANTI MOUSE EGF Biotin

Price:
499 EUR
598 USD
414 GBP
known as: GOAT ANTI MOUSE EGF Biotin
Catalog number: genta-ABS0494
Product Quantity: 50 µg
Category:
Supplier: AbD

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Gene target: egf

Related genes to: GOAT ANTI MOUSE EGF Biotin

Symbol : biotin NIH gene
LocusTag : Bathy11g00270
chromosome : 11
description : biotin synthase
type of gene : protein-coding
Modification date : 2015-06-26
Symbol : egf NIH gene
chromosome : Un
description : epidermal growth factor
type of gene : protein-coding
Other designations : epidermal growth factor (beta-urogastrone)
Modification date : 2015-11-14

Related Pathways to: GOAT ANTI MOUSE EGF Biotin

Gene about :Egf
Pathway :Rn TGF Beta Signaling Pathway
Egf
Gene about :biotin
Pathway :Sc Protein Modifications
biotin

Related product to: GOAT ANTI MOUSE EGF Biotin

Related Articles about: GOAT ANTI MOUSE EGF Biotin

Outcomes of oral biotin treatment in patients with biotinidase deficiency - Twenty years follow-up.

Biotinidase deficiency (BTD) is an inborn error of biotin metabolism inherited as an autosomal recessive trait. Due to the, biotinidase deficiency, biotin is not recycled. Individuals with BTD usually exhibit neurological and cutaneous abnormalities unless treated with biotin. Supplementation with biotin may either ameliorate or if early introduced even prevent symptoms when introduced presymptomatically. - Source :PubMed

Analysis of K-Ras Interactions by Biotin Ligase Tagging.

Mutations of the human K-Ras 4B (K-Ras) G protein are associated with a significant proportion of all human cancers. Despite this fact, a comprehensive analysis of K-Ras interactions is lacking. Our investigations focus on characterization of the K-Ras interaction network. - Source :PubMed

Stress-specific p38 MAP kinase activation is sufficient to drive EGF receptor endocytosis but not nuclear translocation.

P38 MAP kinase-dependent EGF receptor (EGFR) endocytosis is induced by stress. Ligand and stresses like X-rays, reportedly promote nuclear traffic of endocytosed EGFR for regulation of gene transcription and DNA repair. We fail to detect EGFR endocytosis or nuclear transport following X-ray treatment of HeLa or head and neck cancer cells, despite extensive DNA damage induction. Apparent nuclear staining with EGFR extracellular domain antibody remained present despite reduced/absent EGFR expression and so did not represent nuclear EGFR. UVB and UVC, but not X-rays or UVA, induced p38 activation and EGFR endocytosis, though all induced DNA damage, indicating that DNA damage is not sufficient to induce EGFR endocytosis. Increased ROS levels following UVB treatment, compared to X-rays, do not alone explain differences in p38 activation. UVB, like UVC, induced EGFR accumulation predominantly in perinuclear endosomes, rather than the nucleus. Our morphological techniques identifying major changes in receptor distribution do not exclude the possibility that small but biologically relevant amounts of EGFR enter the nucleus. This study highlights the importance and limitations of morphological analyses of receptor distribution in understanding signaling outcome. - Source :PubMed

CBP501 inhibits EGF-dependent cell migration, invasion and epithelial-to-mesenchymal transition of non-small cell lung cancer cells by blocking KRas to Calmodulin binding.

The anti-cancer agent CBP501 binds to calmodulin (CaM). Recent studies showed that migration and metastasis are inhibited by several CaM antagonists. However, there is no available evidence that CBP501 has similar effects. Here we found that CBP501 inhibits migration of non-small cell lung cancer (NSCLC) cells in vitro, even in the presence of migration inducing factors such as WNT, IL-6, and several growth factors. CBP501 also inhibited epidermal growth factor (EGF) enhanced invasion and the epithelial-to-mesenchymal transition (EMT), and this inhibition was accompanied by (i) suppression of Akt and ERK1/2 phosphorylation, and (ii) suppression of expression of transcription factor Zeb1 and the mesenchymal marker Vimentin. A pull down analysis performed using sepharose-immobilized CaM showed that CBP501 blocks the interaction between CaM and KRas. Furthermore, EGF induced Akt activation and cell migration was effectively suppressed by KRas down-regulation in NSCLC cells. Stable knockdown of KRas also made cells insensitive to CBP501's inhibition of growth factor-induced migration. Taken together, these results indicate that CBP501 inhibits binding of CaM with KRas and thereby suppresses the PI3K/AKT pathway, migration, invasion and EMT. These findings have identified a previously unrecognized effect of CBP501 on downstream KRas signaling mechanisms involving EMT and invasion, and provide support for the further clinical development of this agent. - Source :PubMed

Click biotinylation of PLGA template for biotin receptor oriented delivery of doxorubicin hydrochloride in 4T1 cell induced breast cancer.

PLGA was functionalized with PEG and biotin using click chemistry to generate a biotin receptor targeted copolymer (Biotinylated-PEG-PLGA) which in turn was used to fabricate ultrafine nanoparticles (BPNP) of doxorubicin hydrochloride (DOX) for effective delivery in 4T1 cell induced breast cancer. However adequate entrapment of a hydrophilic bioactive like DOX in a hydrophobic polymer system made of PLGA is not usually possible. We therefore modified a conventional W/O/W emulsion method by utilizing ammonium chloride in the external phase to constrain DOX in dissolved polymer phase by supressing its inherent aqueous solubility as per common ion effect. This resulted in over eight fold enhancement in entrapment efficiency of DOX inside BPNP, which otherwise is highly susceptible to leakage due to its relatively high aqueous solubility. TEM and DLS established BPNP to be sized below 100 nm, storage stability studies showed that BPNP were stable for one month at 4°C, and in vitro release suggested significant control in drug release. Extensive in vitro and in vivo studies were conducted to propound anticancer and antiproliferative activity of BPNP. Plasma and tissue distribution study supplemented by pertinent in vivo fluorescence imaging mapped the exact fate of DOX contained inside BPNP once it was administered intravenously. A comparative safety profile via acute toxicity studies in mice was also generated to out rightly establish usefulness of BPNP. Results suggest that BPNP substantially enhance anticancer activity of DOX whilst simultaneously mitigating its toxic potential due to altered spatial and temporal presentation of drug and consequently deserve further allometric iteration. - Source :PubMed

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