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Product Name: IGF-II Antibody
Species Reactivity: Human
Tested Applications: ELISA, Neut, WB
Applications: Neutralization: To yield one-half maximal inhibition [ND50] of the biological activity of hIGF-II (10 ng/mL), a concentration of 3.1 4.6 mg/mL of this antibody is required. ELISA:To detect hIGF-II by direct ELISA (using 100 μL/well antibody solution) a concentration of at least 0.5 μg/mL of this antibody is required. This antigen affinity purified antibody, in conjunction with compatible secondary reagents, allows the detection of 0.2 – 0.4 ng/well of recombinant hIGF-II. Sandwich:To detect hIGF-II by sandwich ELISA (using 100 μL/well antibody solution) a concentration of 0.5 – 2.0 μg/mL of this antibody is required. This antigen affinity purified antibody, in conjunction with our Biotinylated Anti-Human IGF-II (XP-5160Bt) as a detection antibody, allows the detection of at least 0.2 – 0.4 ng/well of recombinant hIGF-II.Western Blot:To detect hIGF-II by Western Blot analysis this antibody can be used at a concentration of 0.1 – 0.2 μg/mL. Used in conjunction with compatible secondary reagents the detection limit for recombinant hIGF-II is 1.5 – 3.0 ng/lane, under either reducing or non-reducing conditions.
User Note: Centrifuge vial prior to opening.
Predicted Molecular Weight:
Immunogen: Produced from sera of rabbits pre-immunized with highly pure (>98%) recombinant hIGF-II (human Insulin Like Growth Factor-II).
Host Species: Rabbit
Purification: Anti-hIGF-II specific antibody was purified by affinity chromatography employing immobilized hIGF-II matrix.
Physical State: Lyophilized
CAS NO.: 854601-70-0
Product: Ebselen
Buffer:
Concentration:
Storage Conditions: IGF-II antibody is stable for at least 2 years from date of receipt at -20˚C. The reconstituted antibody is stable for at least two weeks at 2-8˚C. Frozen aliquots are stable for at least 6 months when stored at -20˚C. Avoid repeated freeze-thaw cycles.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: IGF-II, PP9974, C11orf43Insulin-like growth factor II, Somatomedin-A, IGF-II
Accession NO.: P01344
Protein Ino: 124255
Official Symbol: IGF2
Geneid: 3481
Background:
PubMed ID:http://aac.asm.org/content/25/4/476.abstract

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G 50 of trials, both the AT1 Receptor Agonist review target and distractors were
Y ANOVA test. Posthoc comparisons had been produced employing Student's tY ANOVA test. Posthoc comparisons
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Markers and mechanisms. A single of them, which we termed `PC-Pool', identifies pan-cancer markers as
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Creased thrombin generation (Freudenberger et al., 2009). Besides MPA, one more synthetic gestagen, norethisterone acetate
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Aranodes, and juxtaparanodes. Alterations ofthe axo-glial interaction contribute to the etiology of many neurological diseases.
Eration of JAK2V617F-positive cells [21]. Consequently, combinations that synergisticallyPLOS OneEration of JAK2V617F-positive cells [21]. Therefore,
Microns containing retinyl esters. Irrespective of the mechanism(s) involved, rising vitamin A formation and delivery
Ent the efficacy and adverse effects of this therapeutic trial. Apparently, our patient may possibly
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Ory romance; (RF) Analysis funding; (E) Employment; (ET) Expert testimony; (H) Honoraria acquired; (OI) Ownership
Ble summarize the outcomes of 5 independent experiments right after transfer of 1 to 106105
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The JAKV617E mutation. As tyrosine phosphorylation of STAT proteins inducesThe JAKV617E mutation. As tyrosine phosphorylation
Ptin-induced increase in Gmax was inhibited by siAMPK and CC (Fig. 2F). We also confirmed
Se antioxidants had pretty restricted effects on DNA harm and repair for these iPS cells
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Mp. 1H NMR and 13C NMR spectra were recorded on aMp. 1H NMR and 13C
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Sis pilaris. There was no familial history of cardiac disease. Mutation Evaluation and Haplotype Evaluation
Et al., 1992) to produce vpr/ RAG1+/- mice in F1 generation. The F1 vpr transgenic
Cells showed related final results (Figure 1--figure supplement 1D), indicating that CDCells showed comparable outcomes
Hed by means of modulation of regulatory pathways, attaining an JNK3 site insulin-like impact: augmentingHed
E experiments is identified in Supporting Details. In experiments on NO/nitrite release from bladders, basal
The mechanisms underlying the lower in severity of CIA following administration of GMSCs. GMSC injection
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Bination with paclitaxel (PTX) around the CD44+/CD24-/low CSC population, and determined the worth and feasibility
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Cript.Acknowledgments This study was funded by the H.L. Lauterbach Fund and the NOFAR Grant from
Es Sp1-6 and Sp1-7) was deleted, an further reduction in luciferase activity was observed. These
Entiation and memory formation [51]. Also, RCAN1-1S overexpression within the hippocampal neuronal cell line HT22
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Flow price of 1 mLh). Then, the technique was operated in continuousFlow rate of
Ession, suggesting that the enhanced vascular reactivity to phenylephrine induced byEssion, suggesting that the elevated
Markers and mechanisms. A single of them, which we termed `PC-Pool', identifies pan-cancer markers as
Sembly, 2014 (un.org/en/ga/search/view_doc.asp?symbol=A/ RES/69/1, accessed 25 November 2014). 5. Statistical Tables on Overseas Filipino Workers
Y making use of the Bonferroni strategy to make sure that there were variations among
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Xperiment comparing the polypeptide SDS-PAGE profiles of uninduced and IPTG-induced cultures for F1, LcrV and
Of S. spinosa Lu106 exhibited a development defect relative to that with the wild form.
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Assay from the studied drugs in pure forms and pharmaceutical formulations.Conflicts of InterestsThere is no
Autophagy. Therefore we conclude that vacuolar lipase activity is, for by far the most element,
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Any phenotypic alteration in the adipose tissue of Agtrap??mice under HF loading, and Agtrap??mice indeed
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Nto the pathogenesis of aortic stenosis.AcknowledgmentsFunded by grants from the American Heart Association (AHA: 11GRNT7900016)
G of oxidative phosphorylation, high amplitude mitochondrial swelling and outer membrane rupture (Di Lisa et
That A-ring modifications seem to become tolerable for yielding biologically intriguingThat A-ring modifications seem to
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Ther up-regulated in prostate cancer [9], also as non-prostatic malignancies including gastric cancer [10]. PSCA
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Ysis of pheromone-dependent gene transcription in WT and reg1 cells. CellsYsis of pheromone-dependent gene transcription
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The JAKV617E mutation. As tyrosine phosphorylation of STAT proteins inducesThe JAKV617E mutation. As tyrosine phosphorylation
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Ents: EW ARP HJP AD MG. Analyzed the data: EW AD MG HH AP JGBS.
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Sets we discover that there is a statistical difference (P = 2.eight ?1026), confirming that
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