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Nanog [MD204R]
Product group: | Primary |
Monoclonal/ Polyclonal: | Monoclonal |
Clone: | EP119 |
Host: | Rabbit |
Isotype: | IgG |
Application: | Immunohistochemistry (IHC) |
Application notes: | Prediluted |
Conjugation Type: | Unconjugated |
Reactivity: | Human |
General notes: | Localization: cytoplasm. |
Buffer: | citrate pH6.0 or EDTA pH8.0 |
UNSPSC code: | 12352203 |
Nanog is a homeodomain-containing transcription factor that is involved in the maintenance of pluripotency and self renewal in embryonic stem cells. Nanog expression is controlled by a network of factors including Sox2 and the key pluripotency regulator Oct-4. Recent advances in somatic cell reprogramming have utilized viral expression of combinations of transcription factors including nanog, Oct-4, Sox2, KLF4, c-Myc, and LIN28. Studies show that Nanog expression can be absent in normal adult organ tissues, but presented in undifferentiated germ cell tumors such as seminoma, dysgerminoma and embryonal carcinoma. Nanog may be used as an aid in the determination of undifferentiated tumors of germ cell origin from non-germ cell tumors (Shipping Cost: €200.00)
Survivin [EP119]
Survivin is a unique member of the inhibitor of apoptosis (IAP) protein family that interferes with post-mitochondrial events including activation of caspases. Survivin regulates the cell cycle and is expressed in most tumors, but it is barely detectable in terminally differentiated normal cells and tissues. Survivin is expressed in the G2/M phase of the cell cycle. At the beginning of mitosis, survivin associates with microtubules of the mitotic spindle in a specific and saturable reaction that is regulated by microtubule dynamics. Disruption of survivin-microtubule interactions results in loss of survivin's anti-apoptotic function and increased caspase-3 activity, a mechanism involved in cell death during mitosis. Nuclear-cytoplasmic shuttling of survivin is controlled by nuclear export signal (NES), which is necessary for the anti-apoptotic function of survivin. Inhibition of the NES makes cells more susceptible to chemotherapy- or radiotherapy-induced apoptosis. The association of survivin expression with tumor progression, but not overall patient survival, has been observed in a variety of malignancies including renal cell carcinoma, ovarian carcinoma, hepatocellular carcinoma, prostate carcinoma and breast carcinoma. However, the link between a poor prognosis and nuclear expression of Survivin in tumors is controversial. A literature review of 19 publications that measured nuclear survivin in different cancer types showed the following: 9 studies concluded that nuclear survivin was associated with an unfavorable prognosis, whereas 5 showed a favorable prognosis. The authors concluded that the nuclear pool of survivin is involved in promoting cell proliferation in most (if not all) cases, whereas the cytoplasmic pool of survivin may participate in controlling cell survival but not cell proliferation.
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