IDOL Antibody / MYLIP (F54294)

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IDOL Antibody / MYLIP (F54294) Catalog No. Formulation Size F54294-0.4ML In 1X PBS, pH 7.4, with 0.09% sodium azide 0.4 ml F54294-0.08ML In 1X PBS, pH 7.4, with 0.09% sodium azide 0.08 ml Bulk quote request Availability 1-3 business days Species Reactivity Human, Mouse, Rat Format Purified Clonality Polyclonal (rabbit origin) Isotype Rabbit Ig Purity Antigen affinity purified UniProt Q8WY64 Applications Western blot : 1:500-1:2000 Immunohistochemistry (FFPE) : 1:25 Flow cytometry : 1:25 (1x10e6 cells) Limitations This IDOL antibody is available for research use only. Western blot testing of human 1) 293 and 2) MCF7 cell lysate with IDOL antibody. Predicted molecular weight ~50 kDa. Western blot testing of mouse kidney lysate with IDOL antibody. Predicted molecular weight ~50 kDa. Western blot testing of rat brain lysate with IDOL antibody. Predicted molecular weight ~50 kDa. IHC testing of FFPE human brain tissue with IDOL antibody. HIER: steam section in pH6 citrate buffer for 20 min and allow to cool prior to staining. Flow cytometry testing of fixed and permeabilized human MCF7 cells with IDOL antibody; Blue=isotype control, Green= IDOL antibody. Description The ERM protein family members ezrin, radixin, and moesin are cytoskeletal effector proteins linking actin to membrane-bound proteins at the cell surface. Myosin regulatory light chain interacting protein (MYLIP), also called Inducible degrader of the LDL-receptor (IDOL), is a novel ERM-like protein that interacts with myosin regulatory light chain and inhibits neurite outgrowth. Application Notes The stated application concentrations are suggested starting points. Titration of the IDOL antibody may be required due to differences in protocols and secondary/substrate sensitivity. Immunogen A portion of amino acids 111-139 from the human protein were used as the immunogen for the IDOL antibody. Storage Aliquot the IDOL antibody and store frozen at -20oC or colder. Avoid repeated freeze-thaw cycles. Ordering: Phone:858.663.9055 | Fax:1.267.821.0800 | Email:[email protected] Copyright © NSJ Bioreagents. All rights reserved.

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Activated Ezrin Controls MISP Levels to Ensure Correct Numa Polarization and Spindle Orientation Yvonne T
© 2018. Published by The Company of Biologists Ltd | Journal of Cell Science (2018) 131, jcs214544. doi:10.1242/jcs.214544 RESEARCH ARTICLE Activated ezrin controls MISP levels to ensure correct NuMA polarization and spindle orientation Yvonne T. Kschonsak1,2 and Ingrid Hoffmann1,* ABSTRACT misregulation in spindle orientation can result in disorganized tissue Correct spindle orientation is achieved through signaling pathways that morphology due to cell multi-layering, which could be associated provide a molecular link between the cell cortex and spindle with the earliest cancer developments (McCaffrey and Macara, microtubules in an F-actin-dependent manner. A conserved cortical 2011; Pease and Tirnauer, 2011). protein complex, composed of LGN (also known as GPSM2), NuMA The precise spindle position and orientation in the cell is achieved (also known as NUMA1) and dynein–dynactin, plays a key role in by signaling pathways generating pulling and pushing forces on the establishing proper spindle orientation. It has also been shown that the spindle, both externally or internally (Gönczy, 2002; Grill and actin-binding protein MISP and the ERM family, which are activated by Hyman, 2005; Théry et al., 2005; Fink et al., 2011). The longest lymphocyte-oriented kinase (LOK, also known as STK10) and Ste20- established player in spindle orientation is the conserved ternary α like kinase (SLK) (hereafter, SLK/LOK) in mitosis, regulate spindle complex, composed of G i, Leu-Gly-Asn repeat-enriched protein orientation. Here, we report that MISP functions downstream of the (LGN, also known as GPSM2) and nuclear mitotic apparatus ERM family member ezrin and upstream of NuMA to allow optimal (NuMA, also known as NUMA1) (Du et al., 2001; Du and Macara, α spindle positioning.
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Mir‑200B Regulates Breast Cancer Cell Proliferation and Invasion by Targeting Radixin
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