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Bryos In the early embryo, the cells forming the embryo proper constitute only a minor volume of the embryo compared to the large yolk cell (Fig. 1B). The abundance of yolk proteins interferes with any proteomic application that intends to target the cells of the embryo proper. The major yolk protein Vitellogenin, a phospholipo-glycoprotein,Page 1 of(page number not for citation purposes)BMC Devel
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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura
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Nd on the abundance of the target protein. If the yolk is not removed manually, then only 1 or 2 embryos (50?00 ) can be loaded per lane on a gel to avoid overloading effects due to yolk protein. This limits the sensitivity for cellular proteins. The deyolking method enabled us to load significantly more embryos and therefore the signal from specific cellular proteins was increased.Figure 3 demon
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X Ethnicity (n = 555, 336, 219) White/Caucasian (reference) Unknown/Mixed/ Other Aboriginal Asian Obesity Diabetes mellitus Chronic obstructive pulmonary disease Alcohol abuse Chronic kidney disease Day 1 support, physiology, and laboratory values APACHE II score (n = 508, 306, 202) Invasive mechanical ventilation (n = 553, 338, 215) Inotrope or vasopressor Mean arterial pressure (mmHg) (n = 522,
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R 100 mg/kg Triphala 5 times a week. Our results are consistent with previous studies where Triphala was shown to be effective in suppressing the growth ofPage 10 of(page number not for citation purposes)BMC Cancer 2008, 8:http://www.biomedcentral.com/1471-2407/8/.' .' .' .'0 0.5 1 2 4of cells with DCF fluorescenceS (5. 7KU 7U SS 6HU16 12 8 43 53 FOHDYHGFWLQTPL treatment (hours)1 P0 73/ J PO0.'
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Is transcriptionaly regulated by ERK in response to Triphala treatment suggesting ERK as an upstream regulator of p53 in Capan-2 cells. We also observed that Triphala induce apoptosis by ERK activation in BxPC-3 cells, which has mutated p53. This is in part consistent with the observation that activated ERK lead to apoptosis after DNA damage in a p53 independent manner [49]. On the other hand, Tri
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Few of our U87 galectin1 clones. Parental U87MG cells, along with galectin-1 and acGFP-only clones were injected into the right caudate/putamen complex of nude mice. Tumors overexpressing galectin-1 shortened survival of their hosts compared to their parental counterparts (Figure 5). A few animals (7/20) bearing tumors expressing acGFP alone eventually exhibited neurological symptoms. The examinat
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Expression profile of glioblastoma multiforme invasive phenotype points to new therapeutic targets. Neoplasia 2005, 7:7?6. Zagzag D, Salnikow K, Chiriboga L, Yee H, Lan L, Ali MA, Garcia R, Demaria S, Newcomb EW: Downregulation of major histocompatibility complex antigens in invading glioma cells: stealth invasion of the brain. Lab Invest 2005, 85:328?41. Camby I, Belot N, Rorive S, Lefranc F, Mau

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