추천 제품
생물학적 소스
mouse
Quality Level
항체 형태
culture supernatant
항체 생산 유형
primary antibodies
클론
DE2, monoclonal
종 반응성
monkey, bovine, human
제조업체/상표
Chemicon®
기술
ELISA: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable
동형
IgG
NCBI 수납 번호
UniProt 수납 번호
배송 상태
dry ice
타겟 번역 후 변형
unmodified
유전자 정보
human ... APP(351)
애플리케이션
Anti-Amyloid Antibody, β 1-16, clone DE2 is an antibody against Amyloid for use in ELISA, WB, IH(P).
Western blot: 1:10-1:300 Immunohistochemistry: 1:10-1:200 on formaldehyde fixed, paraffin embedded tissue, requires formic acid or microwave pretreatment to stain Alzheimer′s brain senile plaques. ELISA Immunoprecipitation
Optimal working dilutions must be determined by end user.
Optimal working dilutions must be determined by end user.
물리적 형태
Culture supernatant. Liquid containing 0.02% sodium azide.
법적 정보
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
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.
Acta neuropathologica, 141(5), 651-666 (2021-03-08)
The farnesyltransferase inhibitor, Lonafarnib, reduces tau inclusions and associated atrophy in familial tauopathy models through activation of autophagy, mediated by the inhibition of farnesylation of the Ras GTPase, Rhes. While hinting at a role of Rhes in tau aggregation, it
S100A9 knockout decreases the memory impairment and neuropathology in crossbreed mice of Tg2576 and S100A9 knockout mice model.
Testing null
Proceedings of the National Academy of Sciences of the United States of America, 102(17), 6021-6026 (2005-04-28)
The defining features of the widely conserved HtrA (high temperature requirement) family of serine proteases are the combination of a catalytic protease domain with one or more C-terminal PDZ domains and reversible zymogen activation. Even though HtrAs have previously been
Brain communications, 3(2), fcab079-fcab079 (2021-05-21)
Synaptic degeneration has been reported as one of the best pathological correlates of cognitive deficits in Alzheimer's disease. However, the location of these synaptic alterations within hippocampal sub-regions, the vulnerability of the presynaptic versus postsynaptic compartments, and the biological mechanisms
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