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- goat polyclonal IgG, 200µg/ml
- epitope mapping near the C-terminus of NIPA of human origin
- recommended for detection of NIPA of mouse, rat and human origin by WB, IP, IF and ELISA; also reactive with additional species, including equine, canine and bovine
- blocking peptide, sc-48603 P
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Ordering Information
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| Species |
Gene Name |
Gene ID |
Chromosome Location |
Isoform (mRNA) Accession # |
Protein Accession # |
OMIM™ Number |
| Human |
ZC3HC1 |
51530 |
7q32.2 |
NM_016478 |
Q86WB0
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n/a |
| Mouse |
Zc3hc1 |
232679 |
6 A3.3 |
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Q80YV2
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N/A |
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NIPA Background Information Entry into mitosis is essentially driven by cyclin B1 which is located in the cytoplasm throughout interphase, but accumulates in the nucleus just before mitosis occurs. Nuclear Interaction Partner of ALK (NIPA) plays a critical role in cyclin B1 regulation. NIPA is normally phosphorylated during G2 and M phases, resulting in an accumulation of cyclin B1. When NIPA sheds its attached phosphate, it binds to SCF to form the SCFNIPA complex, a member of the E3 ubiquitin ligases, which ubiquitinates cyclin B1, thereby targeting it to the proteosome for degradation. Therefore, the accumulation of cyclin B1 is due to the inability of phosphorylated NIPA to bind to the molecule SCF, thereby preventing the degradation of cyclin B1. An absence of NIPA causes cyclin B1 to accumulate abnormally, leading to premature mitotic entry, loss of checkpoint control, and genomic instability which are all associated with cancer. The phosphorylated form of NIPA may also be involved in apoptotic signaling pathways. |
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NIPA (C-14)
Click on image to enlarge
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NIPA (C-14): sc-48603. Western blot analysis of NIPA expression in HeLa (A) and WI 38 (B) whole cell lysates.
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