SKA2 antibody was raised against a 15 amino acid peptide from near the amino terminus of human SKA2.
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Target description
Upon entry into mitosis, the cell′s microtubule (MT) network forms the mitotic spindle, allowing the segregation of paired chromosomes. Proteinaceous structures on centromeric chromatin termed kinetochores (KT) are essential for the proper attachment of the chromosomes to the spindle MTs. A recently discovered spindle and kinetochore complex, comprised of proteins SKA1, SKA2, and SKA3, has been found to be required for stable KT-MT interactions and timely anaphase onset. Depletion of either SKA1 or SKA2 by siRNA results in the loss of both proteins from the KT, but does not impact overall KT structure. Cells depleted of the SKA complex undergo a prolonged checkpoint-dependent delay in a metaphase-like state, indicating the importance of the SKA complex in the maintenance of the metaphase plate and spindle checkpoint silencing. SKA2 has also been shown to interact with glucocorticoid receptors and to be involved in glucocorticoid signaling and cell proliferation.
Linkage
The action of this antibody can be blocked using blocking peptide SBP3500102.
Physical form
Supplied at approx. 1 mg/mL in phosphate buffered saline containing 0.02% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
High levels of proinflammatory cytokines induce neurotoxicity and catalyze inflammation-driven neurodegeneration, but the specific release mechanisms from microglia remain elusive. Here we show that secretory autophagy (SA), a non-lytic modality of autophagy for secretion of vesicular cargo, regulates neuroinflammation-mediated neurodegeneration
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