产品编号

产品名称

包装

AG-40B-0138-C050

重组型Fc（人）：Dectin-1（小鼠）
Fc (human):Dectin-1 (mouse) (rec.)

50 ug

产品详情

别名

C型凝集素结构域家族7成员A;   β-葡聚糖受体; 树突状细胞相关C型凝集素1; C型凝集素超家族成员12; DC相关C型凝集素1

产品类别

蛋白

特性

来源/宿主

HEK 293 cells

序列

在人IgG1的Fc部分的C-末端融合了小鼠dectin-1（第72-244位氨基酸）。

交叉反应

小鼠

分子量（MW）

~56kDa   (SDS-PAGE)

纯度

≥95%   (SDS-PAGE)

内毒素含量

<0.01EU/μg纯化蛋白   (LAL测试; Lonza)。

浓度

重溶后为1mg/mL。

配制

用50μL灭菌水复溶。

简述

冻干品。含有PBS。

其他产品数据

UniProt link Q6QLQ4: Dectin-1 (mouse) http://www.uniprot.org/uniprot/Q6QLQ4）

运输及储存

运输

冰袋

短期存储

+4°C

长期存储

-20°C

储存建议

重新配制后，建议分装并储存于-20°C。

避免反复冻融。

使用含有至少0.1％BSA的PBS进行产品稀释。

使用/稳定性 

收到产品后可在-20℃稳定保存至少6个月。

分装后的产品可在-20℃稳定保存最多3个月。

[1]

Quantitative Analysis of Candida Cell Wall Components by Flow Cytometry with Triple-Fluorescence Staining: M.F. Nogueira, et al.; J. Microbiol. Modern Techn. 2, 2017

产品编号

产品名称

包装

AG-40B-0139-C050

重组型Fc（人）：Dectin-2（小鼠）
Fc (human):Dectin-2 (mouse) (rec.)

50 ug

免疫细胞化学：1. see J. Virol. 85, 13019 (2011)

                        2. Nat. Immunol. 13, 255 (2012)

免疫沉淀：in RIPA buffer, see Mol. Cell 49, 331

                 (2012)

免疫组化：1:200, for a protocol see Nature 493, 

                67 (2012)

ChIP assay：2µg/DNA of 10E6 cells

                   (see Nat. Immunol. 16, 859 (2015))

产品编号

产品名称

规格

AG-20B-0006-C100

anti-NLRP3/NALP3    (mouse), mAb (Cryo-1)
     抗小鼠NLRP3/NALP3单抗（Cryo-1）

100 ug

AG-20B-0014-C100

anti-NLRP3/NALP3,    mAb (Cryo-2)
     NLRP3/NALP3单抗（Cryo-2)

100 ug

1.

Thioredoxin-interacting protein links oxidative stress to inflammasome activation: R. Zhou, et al.; Nature Immunology 11, 136 (2010)

2.

The NLRP3 inflammasome promotes renal inflammation and contributes to CKD: A. Vilaysane, et al.; J. Am. Soc. Nephrol. 21, 1732 (2010)

3.

A role for mitochondria in NLRP3 inflammasome activation: R. Zhou, et al.; Nature 469, 221 (2011)

4.

Differential expression of NLRP3 among hematopoietic cells: G. Guarda, et al.; J. Immunol. 186, 2529 (2011)

5.

Mechanism of Impaired NLRP3 Inflammasome Priming by Monophosphoryl Lipid A: C.A. Embry, et al.; Sci. Signal. 4, ra28 (2011)

6.

Measles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleukin-1 Secretion: N. Komune, et al.; J. Virol. 85, 13019 (2011)

7.

Novel role of PKR in inflammasome activation and HMGB1 release: B. Lu, et al.; Nature 488, 670 (2012)

8.

Deubiquitination of NLRP3 by BRCC3 Critically Regulates Inflammasome Activity: B.F. Py, et al.; Mol. Cell 49,331 (2012)

9.

NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice: M.T. Heneka, et al.; Nature 493, 67 (2012)

10.

Activation of autophagy by inflammatory signals limits IL-1b production by targeting ubiquitinated inflammasomes for destruction: C.-S. Shi, et al.; Nat. Immunol. 13, 255 (2012)

11.

Inflammasome-independent NLRP3 augments TGF-β signaling in kidney epithelium: W. Wang, et al.; J. Immunol. 190, 1239 (2013)

12.

Omega-3 Fatty Acids Prevent Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome Activation: Y. Yan, et al.; Immunity 38, 1154 (2013)

13.

LRRFIP2 negatively regulates NLRP3 inflammasome activation in macrophages by promoting Flightless-I-mediated caspase-1 inhibition: J. Jin, et al.; Nat. Commun. 4, 2075 (2013)

14.

Proapoptotic Chemotherapeutic Drugs Induce Noncanonical Processing and Release of IL-1β via Caspase-8 in Dendritic Cells: C. Antonopoulus, et al. J. Immunol. 191, 4789 (2013)

15.

Constitutively activated NLRP3 inflammasome causes inflammation and abnormal skeletal development in mice: S.L. Bonar, et al.; PLoS One 7, e35979 (2012)

16.

FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes: P. Gurung, et al.; J. Immunol. 192, 1835 (2014)

17.

XIAP Restricts TNF- and RIP3-Dependent Cell Death and Inflammasome Activation: M. Yabal, et al.; Cell Rep.7, 1796 (2014)

18.

The adaptor ASC has extracellular and 'prionoid' activities that propagate inflammation: B.S. Franklin, et al.; Nat. Immunol. 15, 727 (2014)

19.

The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response: A. Baroja-Mazo, et al.; Nat. Immunol. 15, 738 (2014)

20.

Toward a chemical marker for inflammatory disease: a fluorescent probe for membrane-localized thioredoxin: M.H. Lee, et al.; JACS 136, 8430 (2014)

21.

Prostaglandin E2 inhibits NLRP3 inflammasome activation through EP4 receptor and intracellular cyclic AMP in human macrophages: M. Sokolowska, et al.; J. Immunol. 194, 5472 (2015)

22.

The receptor NLRP3 is a transcriptional regulator of TH2 differentiation: M. Bruchard, et al.; Nat. Immunol. 16,859 (2015)

23.

NLRP3 Inflammasome Is Expressed and Functional in Mouse Brain Microglia but Not in Astrocytes: A. Gustin, et al.; PLos One 10, e0130624 (2015)

24.

Nlrp6 promotes recovery after peripheral nerve injury independently of inflammasomes: E. Ydens, et al.; J. Neuroinfl. 12, 143 (2015)

25.

The Crohn’s disease risk factor IRGM limits NLRP3 inflammasome activation by impeding its assembly and by mediating its selective autophagy: S. Mehto, et al.; Mol. Cell 73, 429 (2019)

26.

Lack of Protein Prenylation Promotes Nlrp3 Inflammasome Assembly in Human Monocytes: O.P. Skinner, et al.; J. Allergy Clin. Immunol. (Epub ahead of print) (2019)

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

细胞自噬研究 

       自噬（autophagy）是指从粗面内质网的无核糖体附着区脱落的双层膜包裹部分胞质和细胞内需降解的细胞器、蛋白质等成分形成自噬体（autophagosome），并与溶酶体融合形成自噬溶酶体，降解其所包裹的内容物，以实现细胞本身的代谢需要和某些细胞器的更新。自噬是继细胞凋亡（apoptosis）后，当前生命科学最热的研究领域。

自噬过程示意图

ELISA法定量检测自噬标记物——NBR1和p62

       NBR1和p62这两个蛋白的功能类似于支架蛋白，在自噬过程中起着转运和降解蛋白的功能。NBR1和p62 ELISA试剂盒可以灵敏地定量检测人、大鼠、小鼠细胞裂解液中自噬标记物NBR1和p62的含量。此试剂盒具有如下优点：

●　灵敏度高，检测NBR1可低至66pg/ml、p62可低至100pg/ml。

●　简便地操作步骤节省宝贵时间，减少错误。

●　结果比Western Blot更可靠。

●　适用于高通量筛选。

使用p62 ELISA试剂盒检测自噬标记物

图Ａ图Ｂ图Ｃ

       自噬诱导药物处理人乳腺癌细胞。经药物处理6小时和12小时后，细胞裂解，使用p62 ELISA试剂盒定量检测、p62抗体和LC3-II抗体进行免疫印迹。经药物处理后，自噬标记物表达水平有变化，p62蛋白水平降低（A和B图），LC3-II水平上升（C图）

产品信息

产品编号

产品名称

规格

ADI-900-211

NBR1 ELISA Kit

1X96孔

ADI-900-212

p62 ELISA Kit

1X96孔

　产品编号

产品名称

产品编号

产品名称

产品编号

产品名称

ADI-900-138

Bax

ADI-900-133

Bcl-2

ADI-900-152

Erk1/2

ADI-900-106

Phospho Jnk1/2

ADI-900-144

GSK-3β

ADI-EKS-715

HSP70

ADI-EKS-895

HSP90α

ADI-900-123A

Phospho GSK-3β

ALX-850-057

p53

AG-45A-0029

SIRT1

AG-45A-0030

SIRT2

ADI-960-070

p53/MDM2

产品编号

产品名称

规格

BML-2837-0500

Autophagy Library

1 Library

500μl/well

BML-2837-0100

1 Library

100μl/well

　　　　产品编号

产品名称

产品编号

产品名称

BML-CM110

Bafilomycin A1

BML-A275

Rapamycin

ALX-550-087

Clonidine

BML-EI397

SMER28

ALX-550-253

Loperamide

ALX-550-095

Tamoxifen

BML-PI102

MG-132

ALX-550-306

Verapamil

　　　产品编号

产品名称

规格

ENZ-51034

　Cyto-ID™ Green detection kit

1 Kit

ENZ-51005

　Cyto-ID™ Red detection kit (GFP-Certified™)

1 Kit

ENZ-51015

　Cyto-ID™ Red cytotoxicity kit (GFP-Certified™)

1 Kit

ENZ-52252

　MM 4-64 Fluorescent dye for autophagy in yeast

1mg

产品编号

产品名称

规格

　ALX-803-080-C100

　LC3B,mAb(5F10)

100μg

　BML-PW1125-0025

　NBR1(human), pAb

25μl

　ALX-215-065-1

　mTOR(human FRB Domain), pAb

1 vial

　ADI-905-721-100

　Beclin-1, pAb

100μg

　ADI-905-687-100

　mTOR, pAb

100μg

　BML-PW9860-0025

　P62(human), pAb

25μl