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Merck
모든 사진(1)

문서

CBL243

Sigma-Aldrich

Anti-Glucose Transporter GLUT-4 Antibody

Chemicon®, from rabbit

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About This Item

UNSPSC 코드:
12352203
eCl@ss:
32160702
NACRES:
NA.41

생물학적 소스

rabbit

Quality Level

항체 형태

affinity isolated antibody

항체 생산 유형

primary antibodies

클론

polyclonal

정제법

affinity chromatography

종 반응성

mouse, human, rat

제조업체/상표

Chemicon®

기술

immunoprecipitation (IP): suitable
western blot: suitable

NCBI 수납 번호

UniProt 수납 번호

배송 상태

wet ice

타겟 번역 후 변형

unmodified

유전자 정보

human ... SLC2A4(6517)

특이성

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.

면역원

Partially purified GLUT-4

애플리케이션

Research Category
Signaling
Research Sub Category
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.

표적 설명

46 kDa

물리적 형태

ImmunoAffinity Purified
Purified immunoglobulin in PBS with 0.01% sodium azide.

저장 및 안정성

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.

분석 메모

Control
Positive Control: 3T3 L1 adipocyte membranes

기타 정보

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

법적 정보

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

면책조항

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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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.

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문서 라이브러리 방문

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
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
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
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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