Render Target: STATIC
Render Timestamp: 2024-11-22T11:55:48.205Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-08-01 15:23:25.188
Product last modified at: 2024-08-20T12:15:09.363Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-LKB1 (Thr189) Antibody #3054

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Transfected Only
    MW (kDa) 54
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Phospho-LKB1 (Thr189) Antibody detects transfected levels of LKB1 only when phosphorylated at threonine 189. The antibody does not cross-react with LKB1 phosphorylated at other sites.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr189 of human LKB1. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    LKB1 (STK11) is a serine/threonine kinase and tumor suppressor that helps control cell structure, apoptosis and energy homeostasis through regulation of numerous downstream kinases (1,2). A cytosolic protein complex comprised of LKB1, putative kinase STRAD, and the MO25 scaffold protein, activates both AMP-activated protein kinase (AMPK) and several AMPK-related kinases (3). AMPK plays a predominant role as the master regulator of cellular energy homeostasis, controlling downstream effectors that regulate cell growth and apoptosis in response to cellular ATP concentrations (4). LKB1 appears to be phosphorylated in cells at several sites, including human LKB1 at Ser31/325/428 and Thr189/336/363 (5).
    Mutation in the corresponding LKB1 gene causes Peutz-Jeghers syndrome (PJS), an autosomal dominant disorder characterized by benign GI tract polyps and dark skin lesions of the mouth, hands, and feet (6). A variety of other LKB1 gene mutations have been associated with the formation of sporadic cancers in several tissues (7).
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