CBL243
Anti-Glucose Transporter GLUT-4 Antibody
Chemicon®, from rabbit
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
mouse, human, rat
manufacturer/tradename
Chemicon®
technique(s)
immunoprecipitation (IP): suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... SLC2A4(6517)
Specificity
Specific for human glucose transporter-4 from muscle and adipose tissue. The antisera does not cross-react with GLUT-1. The molecular weight of the glucose transporter precipitated by the serum is approximately 46 kDa.
Immunogen
Partially purified GLUT-4
Application
Research Category
Signaling
Signaling
Research Sub Category
Insulin/Energy Signaling
Insulin/Energy Signaling
This Anti-Glucose Transporter GLUT-4 Antibody is validated for use in IP, WB for the detection of Glucose Transporter GLUT-4.
Western blot analysis of GLUT-4 activity in adipose and muscle tissue (5μg/ml)
Immunoprecipitation of GLUT-4 (5μg/ml)
Optimal working dilutions must be determined by the end user.
Immunoprecipitation of GLUT-4 (5μg/ml)
Optimal working dilutions must be determined by the end user.
Target description
46 kDa
Physical form
ImmunoAffinity Purified
Purified immunoglobulin in PBS with 0.01% sodium azide.
Storage and Stability
For use within 1 month of purchase store at +4°C, for long term storage aliquot antibody into small volumes and store at -20°C.
Analysis Note
Control
Positive Control: 3T3 L1 adipocyte membranes
Positive Control: 3T3 L1 adipocyte membranes
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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.
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Description
Pricing
Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Exercise restores insulin, but not adiponectin, response in skeletal muscle of high-fat fed rodents.
Roberto A Gulli et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 303(10), R1062-R1070 (2012-10-12)
High-fat (HF) diets impair skeletal muscle response to the insulin-sensitizing adipokine adiponectin (Ad) in rodents, preceding the development of insulin resistance. Skeletal muscle insulin response in HF-fed rats can be restored with chronic exercise; whether recovery of skeletal muscle Ad
Xiaohua Zheng et al.
PloS one, 15(2), e0223340-e0223340 (2020-02-14)
The Rab GTPase activating protein known as Akt substrate of 160 kDa (AS160 or TBC1D4) regulates insulin-stimulated glucose uptake in skeletal muscle, the heart, and white adipose tissue (WAT). A novel rat AS160-knockout (AS160-KO) was created with CRISPR/Cas9 technology. Because
Haiyan Wang et al.
Journal of applied physiology (Bethesda, Md. : 1985), 132(1), 140-153 (2021-12-10)
Previous studies demonstrated that acute exercise can enhance glucose uptake (GU), γ3-AMP-activated protein kinase (AMPK) activity, and Akt substrate of 160 kDa (AS160) phosphorylation in skeletal muscles from low-fat diet (LFD)- and high-fat diet (HFD)-fed male rats. Because little is
Haiyan Wang et al.
Facets (Ottawa), 7, 774-791 (2022-11-17)
Attenuated skeletal muscle glucose uptake (GU) has been observed with advancing age. It is important to elucidate the mechanisms linked to interventions that oppose this detrimental outcome. Earlier research using young rodents and (or) cultured myocytes reported that treatment with
Naveen Sharma et al.
Biochimica et biophysica acta, 1822(11), 1735-1740 (2012-08-01)
Calorie restriction (CR; ~60% of ad libitum, AL, consumption) improves insulin-stimulated glucose uptake in skeletal muscle. The precise cellular mechanism for this healthful outcome is unknown, but it is accompanied by enhanced insulin-stimulated activation of Akt. Previous research using Akt2-null
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