验证ACE的抑制效果

样本

参考文献

加工豆浆

Alauddin, M., Shirakawa, H., Hiwatashi, K.,   Shimakage, A., Takahashi, S., Shinbo, M. and Komaia, M. : "Processed   soymilk effectively ameliorates blood pressure elevation in spontaneously   hypertensive rats", J. Funct. Foods., 14, 126 (2015).

芦笋

Nakabayashi, R., Yang, Z., Nishizawa, T.,   Mori, T. and Saito, K. : "Top-down Targeted Metabolomics Reveals a Sulfur-Containing   Metabolite with Inhibitory Activity against Angiotensin-Converting Enzyme in   Asparagus officinalis", J. Nat. Prod., 78(5), 1179 (2015).

大和归（东当归）

浅尾浩史等人：大和归的制备过程中血管紧张素I转化酶（ACE）抑制活性和品质特性的变化”，近畿四国四国农业研究，17,9（2010）。

Methomyl

灭多威

Chloroxuron

枯草隆

Imidacloprid

吡虫啉

Mepanipyrim

嘧菌胺

Oxycarboxin

氧化萎锈灵

Triticonazole

灭菌唑

Bendiocarb

恶虫威

Indanofan

茚草酮

Thiodicarb

硫双威灭多威

Tetrachlorvinphos    (CVMP)

杀虫威

Pirimicarb

抗蚜威

Carpropamid

环丙酰菌胺

Methabenzthiazuron

甲基苯噻隆

Imazalil

抑霉唑

Furametpyr

福拉比

Pencycuron

戊菌隆

Azoxystrobin

嘧菌酯

Hexaflumuron

氟铃脲

Methiocarb

灭赐克

Cycloate

灭草特

Acibenzolar-S-methyl

苯并噻二唑

Pentoxazone

环戊恶草酮

Dymron

杀草隆

Oxaziclomefone

去稗安

Cumyluron

苄草隆

Fenoxaprop-ethyl

高恶唑禾草灵

Spinosad

多杀菌素

Flufenoxuron

氟虫脲

Silafluofen

硅醚菊酯

Cycloprothrin

乙氰菊酯

产品编号

产品名

中文名

包装

161-23963

Pesticide Mixture Standard Solution PL-14-2(each    20μg/ml Acetonitrile Solution)

农药混合标准溶液PL-14-2(各20μg/ml乙腈溶液中)

1ml

165-23961

1ml×5A

产品编号

产品名

中文名

包装

161-22961

Pesticide Mixture Standard Solution PL-1-1 (each    20μg/ml Acetone Solution)

农药混合标准溶液 PL-1-1 (各20μg/ml丙酮溶液中)

1ml×5A

167-22963

1ml

164-22973

Pesticide Mixture Standard Solution PL-2-1 (each    20μg/ml Acetone Solution)

农药混合标准溶液 PL-2-1 (各20μg/ml 丙酮溶液中)

1ml

168-22971

1ml×5A

165-24583

Pesticide Mixture Standard Solution PL-3-2 (each    20μg/ml Acetone Solution)

农药混合标准溶液PL-3-2(各20μg/ml丙酮溶液中)

1ml

169-24581

1ml×5A

162-24593

Pesticide Mixture Standard Solution PL-4-2 (each    20μg/ml Acetone Solution)

农药混合标准溶液PL-4-2(各20μg/ml丙酮溶液中)

1ml

166-24591

1ml×5A

165-24603

Pesticide Mixture Standard Solution PL-6-3 (each    20μg/ml Acetone Solution)

农药混合标准溶液PL-6-3(各20μg/ml丙酮溶液中)

1ml

169-24601

1ml×5A

165-23003

Pesticide Mixture Standard Solution PL-5-1 (each    20μg/ml Acetone Solution)

农药混合标准溶液 PL-5-1 (各20μg/ml丙酮溶液中)

1ml

169-23001

1ml×5

163-23021

Pesticide Mixture Standard Solution PL-7-2 (each    20μg/ml Acetonitrile Solution)

农药混合标准溶液 PL-7-2 (各20μg/ml乙腈溶液中)

1ml×5A

169-23023

1ml

162-25311

Pesticide Mixture Standard Solution PL-9-2 (each    20μg/ml Acetone Solution)

农药混合标准溶液 PL-9-2 (各20μg/ml丙酮溶液中)

1ml×5A

168-25313

1ml

160-23031

Pesticide Mixture Standard Solution PL-8-1 (each    20μg/ml Acetonitrile Solution)

农药混合标准溶液PL-8-1 (各20μg/ml乙腈溶液中)

1ml×5A

166-23033

1ml

160-23053

Pesticide Mixture Standard Solution PL-10-1 (each    20μg/ml Acetone Solution)

农药混合标准溶液 PL-10-1 (各20μg/ml丙酮溶液中)

1ml

164-23051

1ml×5A

161-23941

Pesticide Mixture Standard Solution PL-12-1 (each    20μg/ml Acetone Solution)

农药混合标准溶液PL-12-1(各20μg/ml丙酮溶液中)

1ml×5

167-23943

1ml

164-23953

Pesticide Mixture Standard Solution PL-13-1 (each    20μg/ml Acetone Solution)

农药混合标准溶液PL-13-1(各20μg/ml丙酮溶液中)

1ml

168-23951

1ml×5

161-23963

Pesticide Mixture Standard Solution PL-14-2(each    20μg/ml Acetonitrile Solution)

农药混合标准溶液PL-14-2(各20μg/ml乙腈溶液中)

1ml

165-23961

1ml×5A

165-23983

Pesticide Mixture Standard Solution PL-16-2(each    20μg/ml Acetonitrile Solution)

农药混合标准溶液PL-16-2(各20μg/ml 乙腈溶液中)

1ml

169-23981

1ml×5A

Alternative Name:

Amyloid precursor protein, APP neo

Sensitivity:

0.92 pM (range 11.72 – 1500 pM)

Assay Time:

~2 hours

Applications:

ELISA, Colorimetric detection

Application Notes:

For the quantitative determination of human APP ΔC31 in   cell lysate, cerebral spinal fluid, plasma and serum samples. Sequence   alignments indicate multiple species are probable.

Species reactivity:

Human

Shipping:

Blue Ice Not Frozen

Long Term Storage:

+4°C

Kit/Set Contains:

Microtiter Plate, Assay Buffer, Standard, Detector   Antibody, Antibody-HRP-conjugate, TMB Substrate, Stop Solution, Wash Buffer   Concentrate

Scientific Background:

Alzheimer’s disease (AD) is a progressive   neurodegenerative disease characterized by the senile plaques,   neurofibrillary tangles and loss of synapses and neurons. AD has been largely   viewed as a disease of toxicity being mediated by the accumulation of the   amyloid beta (Aβ) peptide as plaques within the brain resulting in damage to   brain cells from the binding of damaging metals, reactive oxygen species   production and direct damage to cellular membranes. Recent research has   suggested that the Aβ peptide is a multifunctional peptide with   non-pathological effects and that its association with AD is in conjunction   with its roles in combination with other proteins such as the amyloid   precursor protein (APP) resulting in the imbalance between the processes of memory   formation and normal forgetting. It is through the interactions of the Aβ   peptide with APP that the Aβ peptide itself can affect normal modulation and   signaling of APP resulting in its indicated role in the pathogenesis of AD   via signaling effects rather than chemical or physical effects.
     There are three major APP isoforms (APP695, APP751 and APP770)   that are formed through alternative splicing of precursor mRNA. APP770   represents the canonical sequence. The APP695 isoform is preferentially   expressed in the central nervous system, while APP770 and APP751 are more   highly expressed in peripheral tissues. It has been demonstrated that the   full length APP695 can be cleaved via caspase at an intracellular site   (Asp664) resulting in the release of a 31 amino acid C-terminal peptide (C31)   from the remaining larger neo-APP fragment (APP ΔC31) with both of these   entities being pro-apoptotic. Immunohistochemical analysis of human brain   tissue demonstrated that this cytoplasmic cleavage occurs 4-fold greater in patients   with AD versus normal patients and that these cleavage products are localized   to plaques and tangles in key areas of the brain affected by the disease. A   single genetic mutation of aspartic acid residue 664 to alanine of APP695 led   to the complete blockage of the C-terminal cleavage in vivo reversing many   characteristics of the AD phenotype in a transgenic mouse model.   Additionally, in cell culture it has been suggested that the neurotoxicity of   Aβ is dependent on the cleavage of APP at Asp664 and the resulting   Aβ-facilitated APP multimerization.

Technical Info/Product Notes:

Application Notes
  A Colorimetric ELISA for   Alzheimer’s Disease Research Enabling Quantification of APP ΔC31 in Cell   Lysates and Cerebrospinal Fluid
 
  Automation of the Enzo APP ΔC31 ELISA kit

UniProt ID:

P05067