重组小鼠OX40/TNFRSF4/CD134蛋白(His-Avi标记) Mouse OX40/TNFRSF4/CD134 Protein

重组小鼠OX40/TNFRSF4/CD134蛋白(His-Avi标记) Mouse OX40/TNFRSF4/CD134 Protein

产品说明书

FAQ

COA

已发表文献

 

性能参数

分子别名(Synonyms)

OX40L receptor; OX40;CD134; ACT-135

表达区间及表达系统(Source)

Mouse OX40/TNFRSF4/CD134 Protein is expressed from HEK293 with His tag and Avi tag at the C-Terminus. It contains Val20-Pro211.[Accession | P47741]

分子量大小(Molecular Weight)

The protein has a predicted MW of 24.2 kDa. Due to glycosylation, the protein migrates to 50-60 kDa based on SDS-PAGE result.

内毒素(Endotoxin)

Less than 1EU per μg by the LAL method.

纯度(Purity)

> 95% as determined by SDS-PAGE

活性(Activity)

ELISA Data: Immobilized Mouse OX40 Ligand, hFc Tag at 5μg/ml (100μl/well) on the plate. Dose response curve for Mouse OX40, His Tag with the EC50 of 0.56μg/ml determined by ELISA.

制剂(Formulation)

Lyophilized from 0.22μm filtered solution in PBS (pH 7.4). Normally 8% trehalose is added as protectant before lyophilization.

重构方法(Reconstitution)

Centrifuge the tube before opening. Reconstituting to a concentration more than 100 μg/ml is recommended. Dissolve the lyophilized protein in distilled water.

 

储存条件

The product should be stored at -25~-15℃ for 1 year from date of receipt.

2-7 days, 2 ~ 8 °C under sterile conditions after reconstitution.

3 -6 months, -85~-65℃ under sterile conditions after reconstitution.

Recommend to aliquot the protein into smaller quantities when first used and avoid repeated freeze-thaw cycles.

 

注意事项

1.Please operate with lab coats and disposable gloves,for your safety.

2.This product is for research use only.

 

性能参数

分子别名(Synonyms)

OX40L receptor; OX40;CD134; ACT-135

表达区间及表达系统(Source)

Mouse OX40/TNFRSF4/CD134 Protein is expressed from HEK293 with His tag and Avi tag at the C-Terminus. It contains Val20-Pro211.[Accession | P47741]

分子量大小(Molecular Weight)

The protein has a predicted MW of 24.2 kDa. Due to glycosylation, the protein migrates to 50-60 kDa based on SDS-PAGE result.

内毒素(Endotoxin)

Less than 1EU per μg by the LAL method.

纯度(Purity)

> 95% as determined by SDS-PAGE

活性(Activity)

ELISA Data: Immobilized Mouse OX40 Ligand, hFc Tag at 5μg/ml (100μl/well) on the plate. Dose response curve for Mouse OX40, His Tag with the EC50 of 0.56μg/ml determined by ELISA.

制剂(Formulation)

Lyophilized from 0.22μm filtered solution in PBS (pH 7.4). Normally 8% trehalose is added as protectant before lyophilization.

重构方法(Reconstitution)

Centrifuge the tube before opening. Reconstituting to a concentration more than 100 μg/ml is recommended. Dissolve the lyophilized protein in distilled water.

 

储存条件

The product should be stored at -25~-15℃ for 1 year from date of receipt.

2-7 days, 2 ~ 8 °C under sterile conditions after reconstitution.

3 -6 months, -85~-65℃ under sterile conditions after reconstitution.

Recommend to aliquot the protein into smaller quantities when first used and avoid repeated freeze-thaw cycles.

 

注意事项

1.Please operate with lab coats and disposable gloves,for your safety.

2.This product is for research use only.

人源氧化低密度脂蛋白 Human Ox-LDL|Human Oxidized Low Density Lipoprotein(Human Ox-LDL)

人源氧化低密度脂蛋白 Human Ox-LDL|Human Oxidized Low Density Lipoprotein(Human Ox-LDL)

产品说明书

FAQ

COA

已发表文献

产品描述

LDL是由极低密度脂蛋白(VLDL)转变而来,主要功能是把胆固醇运输到全身各处细胞,运输到肝脏合成胆酸,其可用于研究受体介导的内吞作用过程,尤其是在动脉粥样硬化等疾病中,其血浆来源的LDL可用于研究LDL在功能和代谢中的氧化作用。

氧化的LDLOx-LDL)是修饰LDL中的一类。修饰的LDL除包括氧化修饰的LDL外,还包括乙酰化LDL及丙二醛(MDA)、4-羟烯酸(4-HNE)直接结合的LDL,这些未经氧化修饰而仅经一般化学修饰的LDL称为衍化的LDL。不同于衍化的LDLOx-LDL的生理学独特性表现在:1)在细胞生理功能影响上,Ox-LDL可影响花生四烯酸的代谢,抑制胆固醇酯化作用等,但衍化的LDL无上述效应;2Ox-LDL消耗LDL内源性抗氧化物质,使LDL上的维生素E含量下降,而MDA-LDL无上述效应;3)氧化修饰涉及脂质过氧化反应,LDL中的PUFAs被氧化。MDALDL修饰,是直接和ApoB-100结合成希夫氏碱,脂质过氧化反应轻微;4)氧化LDL在氧化程度低时,ApoB降解;在氧化程度高时,ApoB又可发生再聚合。MDALDL的修饰,ApoB无降解、聚合反应发生;5Ox-LDL产生的荧光峰波长为430 nm,而MDA -LDL的荧光峰波长为460 nmOx-LDL不经LDL受体代谢,由清道夫受体识别、结合、内吞饮入细胞并丧失正常的胆固醇代谢途径,引起细胞内脂质沉积,泡沫样变。

LDL氧化修饰的方式有很多种,常见的有:1)细胞介导的LDL氧化修饰,又称为生物氧化修饰的LDL。如内皮细胞,巨噬细胞,单核细胞都具有此功能;2)过度金属离子介导的LDL氧化修饰,如Ca2+Fe2+等;还有其他形式的氧化修饰,包括物理方法如紫外线,或过氧化物酶催化。

YEASEN提供的人源氧化低密度脂蛋白(Human Oxidized Low Density LipoproteinOx-LDL),是由过度铜离子介导人血浆来源的LDL进行的氧化修饰。新鲜血浆经检测为HCVHBsAgHIV阴性。本产品为无菌包装,可以直接稀释使用。Ox-LDL广泛用于脂质代谢的研究较少诱导细胞凋亡。另外我们还提供High Ox-LDL(货号20608JP03)可产生明显的氧化应激,能够用来诱导细胞凋亡,并建立细胞损伤模型。除提供Ox-LDL,我们还提供人源乙酰化LDLAc-LDL),以及荧光标记的LDL 

制备方法

在含10 μM Cu2SO4PBS溶液中氧化人LDL,加入过量的EDTA终止氧化反应。

 

产品性质

蛋白纯度(Purity

97%(琼脂糖凝胶电泳)

蛋白浓度(Concentration

1.0~3.9 mg/mLLowry法)

外观(Appearance

无色乳状液体

缓冲液配方(Buffer Formulation

0.1 μM EDTA-Na2 in PBS, pH 7.4

氧化程度(Oxidized Ratio

TBARS检测(根据MDA的含量反映LDL的氧化程度)

起始LDL0.1~0.5 nmol MDA/mg蛋白

Ox-LDL20~26 nmol MDA/mg蛋白

 

稀释方法

根据实验需要用PBS磷酸盐缓冲液或细胞培养液稀释即可。

 

运输与保存方法

冰袋运输。4℃保存,建议避光,保存时间不要超过6周。千万不可冻存!!

 

注意事项

1)该产品经长期保存后会看到少量沉淀,属于正常现象。低速离心1 ~2 min去除沉淀物,得到澄清液。

2Ox-LDL工作液很不稳定,强烈建议根据单次需要用量,新鲜配置工作液。

3)为了您的安全和健康,请穿实验服并戴一次性手套操作。

4本产品仅作科研用途!

 

HB210830

Q:该产品与 20604 区别是什么?

A:该产品主要研究 LDL 在功能和代谢中的氧化作用;而 20604 主要研究乙酰化作用。

Q:该产品的缓冲液是多少?

A10 μM Cu2SO4 的PBS 溶液。

Q:如何终止产品的氧化反应?

A:加入过量的 EDTA。

Q:该产品长期保存会出现少量沉淀,还可以使用吗?

A:这是正常现象。低速离心 1 ~2min 去除沉淀物,即得到澄清液。

[1] Zhang H, Ge S, Ni B, et al. Augmenting ATG14 alleviates atherosclerosis and inhibits inflammation via promotion of autophagosome-lysosome fusion in macrophages. Autophagy. 2021;17(12):4218-4230. doi:10.1080/15548627.2021.1909833(IF:16.016)
[2] Kai H, Wu Q, Yin R, et al. LncRNA NORAD Promotes Vascular Endothelial Cell Injury and Atherosclerosis Through Suppressing VEGF Gene Transcription via Enhancing H3K9 Deacetylation by Recruiting HDAC6. Front Cell Dev Biol. 2021;9:701628. Published 2021 Jul 9. doi:10.3389/fcell.2021.701628(IF:6.684)
[3] Tao J, Qiu J, Lu L, et al. ZBTB20 Positively Regulates Oxidative Stress, Mitochondrial Fission, and Inflammatory Responses of ox-LDL-Induced Macrophages in Atherosclerosis. Oxid Med Cell Longev. 2021;2021:5590855. Published 2021 Mar 9. doi:10.1155/2021/5590855(IF:6.543)
[4] Wang Y, Xu Z, Wang X, et al. Extracellular-vesicle containing miRNA-503-5p released by macrophages contributes to atherosclerosis. Aging (Albany NY). 2021;13(8):12239-12257. doi:10.18632/aging.103855(IF:5.682)
[5] Zhang Y, Xu X, Ma J, et al. Loss of CD226 protects apolipoprotein E-deficient mice from diet-induced atherosclerosis. Biochim Biophys Acta Mol Basis Dis. 2022;1868(9):166452. doi:10.1016/j.bbadis.2022.166452(IF:5.187)
[6] Keping Y, Yunfeng S, Pengzhuo X, Liang L, Chenhong X, Jinghua M. Sestrin1 inhibits oxidized low-density lipoprotein-induced activation of NLRP3 inflammasome in macrophages in a murine atherosclerosis model. Eur J Immunol. 2020;50(8):1154-1166. doi:10.1002/eji.201948427(IF:4.404)
[7] Wang Y, Jia Q, Zhang Y, Wei J, Liu P. Amygdalin Attenuates Atherosclerosis and Plays an Anti-Inflammatory Role in ApoE Knock-Out Mice and Bone Marrow-Derived Macrophages. Front Pharmacol. 2020;11:590929. Published 2020 Oct 29. doi:10.3389/fphar.2020.590929(IF:4.225)
[8] Zhi H, Wu JP, Lu LM, et al. Decabromodiphenyl ether (BDE-209) enhances foam cell formation in human macrophages via augmenting Toll-like receptor 4-dependent lipid uptake. Food Chem Toxicol. 2018;121:367-373. doi:10.1016/j.fct.2018.09.024(IF:3.977)
[9] Zhi H, Yuan N, Wu JP, et al. MicroRNA-21 attenuates BDE-209-induced lipid accumulation in THP-1 macrophages by downregulating Toll-like receptor 4 expression. Food Chem Toxicol. 2019;125:71-77. doi:10.1016/j.fct.2018.12.044(IF:3.977)
[10] Wu T, Xu W, Wang Y, et al. OxLDL enhances choroidal neovascularization lesion through inducing vascular endothelium to mesenchymal transition process and angiogenic factor expression. Cell Signal. 2020;70:109571. doi:10.1016/j.cellsig.2020.109571(IF:3.968)
[11] Long J, Chen J, Wang Q, et al. NFAT activating protein with ITAM motif 1 (NFAM1) is upregulated on circulating monocytes in coronary artery disease and potentially correlated with monocyte chemotaxis. Atherosclerosis. 2020;307:39-51. doi:10.1016/j.atherosclerosis.2020.06.001(IF:3.919)
[12] Sun L, Gai J, Shi S, et al. Protease-Activated Receptor 2 (PAR-2) Antagonist AZ3451 Mitigates Oxidized Low-Density Lipoprotein (Ox-LDL)-Induced Damage and Endothelial Inflammation. Chem Res Toxicol. 2021;34(10):2202-2208. doi:10.1021/acs.chemrestox.1c00154(IF:3.739)
[13] Huang Z, Li P, Wu L, et al. Hsa_circ_0029589 knockdown inhibits the proliferation, migration and invasion of vascular smooth muscle cells via regulating miR-214-3p and STIM1. Life Sci. 2020;259:118251. doi:10.1016/j.lfs.2020.118251(IF:3.647)
[14] Wang P, Yin B, Zhang Z, et al. Foamy macrophages potentially inhibit tuberculous wound healing by inhibiting the TLRs/NF-κB signalling pathway. Wound Repair Regen. 2022;30(3):376-396. doi:10.1111/wrr.13006(IF:3.617)
[15] Zhou YH, Tang YZ, Guo LY, et al. Overexpression of sFlt-1 represses ox-LDL-induced injury of HUVECs by activating autophagy via PI3K/AKT/mTOR pathway. Microvasc Res. 2022;139:104252. doi:10.1016/j.mvr.2021.104252(IF:3.514)
[16] Liu Y, Sun Y, Bai X, Li L, Zhu G. Albiflorin Alleviates Ox-LDL-Induced Human Umbilical Vein Endothelial Cell Injury through IRAK1/TAK1 Pathway. Biomed Res Int. 2022;2022:6584645. Published 2022 May 13. doi:10.1155/2022/6584645(IF:3.411)
[17] Zang YH, Chen D, Zhou B, et al. FNDC5 inhibits foam cell formation and monocyte adhesion in vascular smooth muscle cells via suppressing NFκB-mediated NLRP3 upregulation. Vascul Pharmacol. 2019;121:106579. doi:10.1016/j.vph.2019.106579(IF:3.330)
[18] Fang M, Li Y, Wu Y, Ning Z, Wang X, Li X. miR-185 silencing promotes the progression of atherosclerosis via targeting stromal interaction molecule 1. Cell Cycle. 2019;18(6-7):682-695. doi:10.1080/15384101.2019.1580493(IF:3.259)
[19] Han R, Luo J, Wang L, Li L, Zheng H. miR-33a-5p Suppresses ox-LDL-Stimulated Calcification of Vascular Smooth Muscle Cells by Targeting METTL3. Cardiovasc Toxicol. 2021;21(9):737-746. doi:10.1007/s12012-021-09663-0(IF:3.239)
[20] Zhang Y, Feng X, Du M, Ding J, Liu P. Salvianolic acid B attenuates the inflammatory response in atherosclerosis by regulating MAPKs/ NF-κB signaling pathways in LDLR-/- mice and RAW264.7 cells. Int J Immunopathol Pharmacol. 2022;36:3946320221079468. doi:10.1177/03946320221079468(IF:3.219)
[21] Xiong X, Yan Z, Jiang W, Jiang X. ETS variant transcription factor 6 enhances oxidized low-density lipoprotein-induced inflammatory response in atherosclerotic macrophages via activating NF-κB signaling. Int J Immunopathol Pharmacol. 2022;36:20587384221076472. doi:10.1177/20587384221076472(IF:3.219)
[22] Li X, Cao Q, Wang Y, Wang Y. Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages [retracted in:  RSC Adv. 2021 Jan 28;11(9):5241]. RSC Adv. 2019;9(71):41709-41719. Published 2019 Dec 17. doi:10.1039/c9ra08322g(IF:3.049)
[23] Gao F, Zhao Y, Zhang B, et al. SJPN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling. Mol Med Rep. 2022;25(5):161. doi:10.3892/mmr.2022.12678(IF:2.952)
[24] Pan Z, Zhang Y, Li C, et al. MiR-296-5p ameliorates deep venous thrombosis by inactivating S100A4. Exp Biol Med (Maywood). 2021;246(21):2259-2268. doi:10.1177/15353702211023034(IF:2.691)
[25] Meng Q, Liu H, Wu H, et al. A Network Pharmacology Study to Explore the Underlying Mechanism of Safflower (Carthamus tinctorius L.) in the Treatment of Coronary Heart Disease. Evid Based Complement Alternat Med. 2022;2022:3242015. Published 2022 May 14. doi:10.1155/2022/3242015(IF:2.630)
[26] Wu YT, Li JB, Lin HQ, et al. Inhibition of miR-200b-3p alleviates lipid accumulation and promotes cholesterol efflux by targeting ABCA1 in macrophage-derived foam cells. Exp Ther Med. 2021;22(2):831. doi:10.3892/etm.2021.10263(IF:2.447)
[27] Li W, Li Y, Zhi W, et al. Diagnostic value of using exosome-derived cysteine-rich protein 61 as biomarkers for acute coronary syndrome. Exp Ther Med. 2021;22(6):1437. doi:10.3892/etm.2021.10872(IF:2.447)
[28] Wang L, Li C, Feng C, Zang Y. YY1 affects the levels and function of fibulin-5 in ox-LDL-treated vascular smooth muscle cells. Exp Ther Med. 2022;23(6):407. doi:10.3892/etm.2022.11334(IF:2.447)
[29] Wei J, Huang L, Li D, et al. Total Flavonoids of Engelhardia roxburghiana Wall. Leaves Alleviated Foam Cells Formation through AKT/mTOR-Mediated Autophagy in the Progression of Atherosclerosis. Chem Biodivers. 2021;18(9):e2100308. doi:10.1002/cbdv.202100308(IF:2.408)
[30] Dong H, Jiang G, Zhang J, Kang Y. LncRNA OIP5-AS1 promotes the proliferation and migration of vascular smooth muscle cells via regulating miR-141-3p/HMGB1 pathway. Am J Med Sci. 2022;363(6):538-547. doi:10.1016/j.amjms.2022.02.012(IF:2.378)
[31] Su G, Sun G, Lv J, et al. Hsa_circ_0004831 downregulation is partially responsible for atorvastatinalleviated human umbilical vein endothelial cell injuries induced by ox-LDL through targeting the miR-182-5p/CXCL12 axis. BMC Cardiovasc Disord. 2021;21(1):221. Published 2021 May 1. doi:10.1186/s12872-021-01998-4(IF:2.298)
[32] Ma G, Bi S, Zhang P. Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells. BMC Cardiovasc Disord. 2021;21(1):248. Published 2021 May 20. doi:10.1186/s12872-021-02048-9(IF:2.298)

产品描述

LDL是由极低密度脂蛋白(VLDL)转变而来,主要功能是把胆固醇运输到全身各处细胞,运输到肝脏合成胆酸,其可用于研究受体介导的内吞作用过程,尤其是在动脉粥样硬化等疾病中,其血浆来源的LDL可用于研究LDL在功能和代谢中的氧化作用。

氧化的LDLOx-LDL)是修饰LDL中的一类。修饰的LDL除包括氧化修饰的LDL外,还包括乙酰化LDL及丙二醛(MDA)、4-羟烯酸(4-HNE)直接结合的LDL,这些未经氧化修饰而仅经一般化学修饰的LDL称为衍化的LDL。不同于衍化的LDLOx-LDL的生理学独特性表现在:1)在细胞生理功能影响上,Ox-LDL可影响花生四烯酸的代谢,抑制胆固醇酯化作用等,但衍化的LDL无上述效应;2Ox-LDL消耗LDL内源性抗氧化物质,使LDL上的维生素E含量下降,而MDA-LDL无上述效应;3)氧化修饰涉及脂质过氧化反应,LDL中的PUFAs被氧化。MDALDL修饰,是直接和ApoB-100结合成希夫氏碱,脂质过氧化反应轻微;4)氧化LDL在氧化程度低时,ApoB降解;在氧化程度高时,ApoB又可发生再聚合。MDALDL的修饰,ApoB无降解、聚合反应发生;5Ox-LDL产生的荧光峰波长为430 nm,而MDA -LDL的荧光峰波长为460 nmOx-LDL不经LDL受体代谢,由清道夫受体识别、结合、内吞饮入细胞并丧失正常的胆固醇代谢途径,引起细胞内脂质沉积,泡沫样变。

LDL氧化修饰的方式有很多种,常见的有:1)细胞介导的LDL氧化修饰,又称为生物氧化修饰的LDL。如内皮细胞,巨噬细胞,单核细胞都具有此功能;2)过度金属离子介导的LDL氧化修饰,如Ca2+Fe2+等;还有其他形式的氧化修饰,包括物理方法如紫外线,或过氧化物酶催化。

YEASEN提供的人源氧化低密度脂蛋白(Human Oxidized Low Density LipoproteinOx-LDL),是由过度铜离子介导人血浆来源的LDL进行的氧化修饰。新鲜血浆经检测为HCVHBsAgHIV阴性。本产品为无菌包装,可以直接稀释使用。Ox-LDL广泛用于脂质代谢的研究较少诱导细胞凋亡。另外我们还提供High Ox-LDL(货号20608JP03)可产生明显的氧化应激,能够用来诱导细胞凋亡,并建立细胞损伤模型。除提供Ox-LDL,我们还提供人源乙酰化LDLAc-LDL),以及荧光标记的LDL 

制备方法

在含10 μM Cu2SO4PBS溶液中氧化人LDL,加入过量的EDTA终止氧化反应。

 

产品性质

蛋白纯度(Purity

97%(琼脂糖凝胶电泳)

蛋白浓度(Concentration

1.0~3.9 mg/mLLowry法)

外观(Appearance

无色乳状液体

缓冲液配方(Buffer Formulation

0.1 μM EDTA-Na2 in PBS, pH 7.4

氧化程度(Oxidized Ratio

TBARS检测(根据MDA的含量反映LDL的氧化程度)

起始LDL0.1~0.5 nmol MDA/mg蛋白

Ox-LDL20~26 nmol MDA/mg蛋白

 

稀释方法

根据实验需要用PBS磷酸盐缓冲液或细胞培养液稀释即可。

 

运输与保存方法

冰袋运输。4℃保存,建议避光,保存时间不要超过6周。千万不可冻存!!

 

注意事项

1)该产品经长期保存后会看到少量沉淀,属于正常现象。低速离心1 ~2 min去除沉淀物,得到澄清液。

2Ox-LDL工作液很不稳定,强烈建议根据单次需要用量,新鲜配置工作液。

3)为了您的安全和健康,请穿实验服并戴一次性手套操作。

4本产品仅作科研用途!

 

HB210830

Q:该产品与 20604 区别是什么?

A:该产品主要研究 LDL 在功能和代谢中的氧化作用;而 20604 主要研究乙酰化作用。

Q:该产品的缓冲液是多少?

A10 μM Cu2SO4 的PBS 溶液。

Q:如何终止产品的氧化反应?

A:加入过量的 EDTA。

Q:该产品长期保存会出现少量沉淀,还可以使用吗?

A:这是正常现象。低速离心 1 ~2min 去除沉淀物,即得到澄清液。

[1] Zhang H, Ge S, Ni B, et al. Augmenting ATG14 alleviates atherosclerosis and inhibits inflammation via promotion of autophagosome-lysosome fusion in macrophages. Autophagy. 2021;17(12):4218-4230. doi:10.1080/15548627.2021.1909833(IF:16.016)
[2] Kai H, Wu Q, Yin R, et al. LncRNA NORAD Promotes Vascular Endothelial Cell Injury and Atherosclerosis Through Suppressing VEGF Gene Transcription via Enhancing H3K9 Deacetylation by Recruiting HDAC6. Front Cell Dev Biol. 2021;9:701628. Published 2021 Jul 9. doi:10.3389/fcell.2021.701628(IF:6.684)
[3] Tao J, Qiu J, Lu L, et al. ZBTB20 Positively Regulates Oxidative Stress, Mitochondrial Fission, and Inflammatory Responses of ox-LDL-Induced Macrophages in Atherosclerosis. Oxid Med Cell Longev. 2021;2021:5590855. Published 2021 Mar 9. doi:10.1155/2021/5590855(IF:6.543)
[4] Wang Y, Xu Z, Wang X, et al. Extracellular-vesicle containing miRNA-503-5p released by macrophages contributes to atherosclerosis. Aging (Albany NY). 2021;13(8):12239-12257. doi:10.18632/aging.103855(IF:5.682)
[5] Zhang Y, Xu X, Ma J, et al. Loss of CD226 protects apolipoprotein E-deficient mice from diet-induced atherosclerosis. Biochim Biophys Acta Mol Basis Dis. 2022;1868(9):166452. doi:10.1016/j.bbadis.2022.166452(IF:5.187)
[6] Keping Y, Yunfeng S, Pengzhuo X, Liang L, Chenhong X, Jinghua M. Sestrin1 inhibits oxidized low-density lipoprotein-induced activation of NLRP3 inflammasome in macrophages in a murine atherosclerosis model. Eur J Immunol. 2020;50(8):1154-1166. doi:10.1002/eji.201948427(IF:4.404)
[7] Wang Y, Jia Q, Zhang Y, Wei J, Liu P. Amygdalin Attenuates Atherosclerosis and Plays an Anti-Inflammatory Role in ApoE Knock-Out Mice and Bone Marrow-Derived Macrophages. Front Pharmacol. 2020;11:590929. Published 2020 Oct 29. doi:10.3389/fphar.2020.590929(IF:4.225)
[8] Zhi H, Wu JP, Lu LM, et al. Decabromodiphenyl ether (BDE-209) enhances foam cell formation in human macrophages via augmenting Toll-like receptor 4-dependent lipid uptake. Food Chem Toxicol. 2018;121:367-373. doi:10.1016/j.fct.2018.09.024(IF:3.977)
[9] Zhi H, Yuan N, Wu JP, et al. MicroRNA-21 attenuates BDE-209-induced lipid accumulation in THP-1 macrophages by downregulating Toll-like receptor 4 expression. Food Chem Toxicol. 2019;125:71-77. doi:10.1016/j.fct.2018.12.044(IF:3.977)
[10] Wu T, Xu W, Wang Y, et al. OxLDL enhances choroidal neovascularization lesion through inducing vascular endothelium to mesenchymal transition process and angiogenic factor expression. Cell Signal. 2020;70:109571. doi:10.1016/j.cellsig.2020.109571(IF:3.968)
[11] Long J, Chen J, Wang Q, et al. NFAT activating protein with ITAM motif 1 (NFAM1) is upregulated on circulating monocytes in coronary artery disease and potentially correlated with monocyte chemotaxis. Atherosclerosis. 2020;307:39-51. doi:10.1016/j.atherosclerosis.2020.06.001(IF:3.919)
[12] Sun L, Gai J, Shi S, et al. Protease-Activated Receptor 2 (PAR-2) Antagonist AZ3451 Mitigates Oxidized Low-Density Lipoprotein (Ox-LDL)-Induced Damage and Endothelial Inflammation. Chem Res Toxicol. 2021;34(10):2202-2208. doi:10.1021/acs.chemrestox.1c00154(IF:3.739)
[13] Huang Z, Li P, Wu L, et al. Hsa_circ_0029589 knockdown inhibits the proliferation, migration and invasion of vascular smooth muscle cells via regulating miR-214-3p and STIM1. Life Sci. 2020;259:118251. doi:10.1016/j.lfs.2020.118251(IF:3.647)
[14] Wang P, Yin B, Zhang Z, et al. Foamy macrophages potentially inhibit tuberculous wound healing by inhibiting the TLRs/NF-κB signalling pathway. Wound Repair Regen. 2022;30(3):376-396. doi:10.1111/wrr.13006(IF:3.617)
[15] Zhou YH, Tang YZ, Guo LY, et al. Overexpression of sFlt-1 represses ox-LDL-induced injury of HUVECs by activating autophagy via PI3K/AKT/mTOR pathway. Microvasc Res. 2022;139:104252. doi:10.1016/j.mvr.2021.104252(IF:3.514)
[16] Liu Y, Sun Y, Bai X, Li L, Zhu G. Albiflorin Alleviates Ox-LDL-Induced Human Umbilical Vein Endothelial Cell Injury through IRAK1/TAK1 Pathway. Biomed Res Int. 2022;2022:6584645. Published 2022 May 13. doi:10.1155/2022/6584645(IF:3.411)
[17] Zang YH, Chen D, Zhou B, et al. FNDC5 inhibits foam cell formation and monocyte adhesion in vascular smooth muscle cells via suppressing NFκB-mediated NLRP3 upregulation. Vascul Pharmacol. 2019;121:106579. doi:10.1016/j.vph.2019.106579(IF:3.330)
[18] Fang M, Li Y, Wu Y, Ning Z, Wang X, Li X. miR-185 silencing promotes the progression of atherosclerosis via targeting stromal interaction molecule 1. Cell Cycle. 2019;18(6-7):682-695. doi:10.1080/15384101.2019.1580493(IF:3.259)
[19] Han R, Luo J, Wang L, Li L, Zheng H. miR-33a-5p Suppresses ox-LDL-Stimulated Calcification of Vascular Smooth Muscle Cells by Targeting METTL3. Cardiovasc Toxicol. 2021;21(9):737-746. doi:10.1007/s12012-021-09663-0(IF:3.239)
[20] Zhang Y, Feng X, Du M, Ding J, Liu P. Salvianolic acid B attenuates the inflammatory response in atherosclerosis by regulating MAPKs/ NF-κB signaling pathways in LDLR-/- mice and RAW264.7 cells. Int J Immunopathol Pharmacol. 2022;36:3946320221079468. doi:10.1177/03946320221079468(IF:3.219)
[21] Xiong X, Yan Z, Jiang W, Jiang X. ETS variant transcription factor 6 enhances oxidized low-density lipoprotein-induced inflammatory response in atherosclerotic macrophages via activating NF-κB signaling. Int J Immunopathol Pharmacol. 2022;36:20587384221076472. doi:10.1177/20587384221076472(IF:3.219)
[22] Li X, Cao Q, Wang Y, Wang Y. Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages [retracted in:  RSC Adv. 2021 Jan 28;11(9):5241]. RSC Adv. 2019;9(71):41709-41719. Published 2019 Dec 17. doi:10.1039/c9ra08322g(IF:3.049)
[23] Gao F, Zhao Y, Zhang B, et al. SJPN1 attenuates the Ox‑LDL‑induced inflammation, apoptosis and endothelial‑mesenchymal transition of human umbilical vein endothelial cells by regulating AMPK/SIRT1/LOX1 signaling. Mol Med Rep. 2022;25(5):161. doi:10.3892/mmr.2022.12678(IF:2.952)
[24] Pan Z, Zhang Y, Li C, et al. MiR-296-5p ameliorates deep venous thrombosis by inactivating S100A4. Exp Biol Med (Maywood). 2021;246(21):2259-2268. doi:10.1177/15353702211023034(IF:2.691)
[25] Meng Q, Liu H, Wu H, et al. A Network Pharmacology Study to Explore the Underlying Mechanism of Safflower (Carthamus tinctorius L.) in the Treatment of Coronary Heart Disease. Evid Based Complement Alternat Med. 2022;2022:3242015. Published 2022 May 14. doi:10.1155/2022/3242015(IF:2.630)
[26] Wu YT, Li JB, Lin HQ, et al. Inhibition of miR-200b-3p alleviates lipid accumulation and promotes cholesterol efflux by targeting ABCA1 in macrophage-derived foam cells. Exp Ther Med. 2021;22(2):831. doi:10.3892/etm.2021.10263(IF:2.447)
[27] Li W, Li Y, Zhi W, et al. Diagnostic value of using exosome-derived cysteine-rich protein 61 as biomarkers for acute coronary syndrome. Exp Ther Med. 2021;22(6):1437. doi:10.3892/etm.2021.10872(IF:2.447)
[28] Wang L, Li C, Feng C, Zang Y. YY1 affects the levels and function of fibulin-5 in ox-LDL-treated vascular smooth muscle cells. Exp Ther Med. 2022;23(6):407. doi:10.3892/etm.2022.11334(IF:2.447)
[29] Wei J, Huang L, Li D, et al. Total Flavonoids of Engelhardia roxburghiana Wall. Leaves Alleviated Foam Cells Formation through AKT/mTOR-Mediated Autophagy in the Progression of Atherosclerosis. Chem Biodivers. 2021;18(9):e2100308. doi:10.1002/cbdv.202100308(IF:2.408)
[30] Dong H, Jiang G, Zhang J, Kang Y. LncRNA OIP5-AS1 promotes the proliferation and migration of vascular smooth muscle cells via regulating miR-141-3p/HMGB1 pathway. Am J Med Sci. 2022;363(6):538-547. doi:10.1016/j.amjms.2022.02.012(IF:2.378)
[31] Su G, Sun G, Lv J, et al. Hsa_circ_0004831 downregulation is partially responsible for atorvastatinalleviated human umbilical vein endothelial cell injuries induced by ox-LDL through targeting the miR-182-5p/CXCL12 axis. BMC Cardiovasc Disord. 2021;21(1):221. Published 2021 May 1. doi:10.1186/s12872-021-01998-4(IF:2.298)
[32] Ma G, Bi S, Zhang P. Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells. BMC Cardiovasc Disord. 2021;21(1):248. Published 2021 May 20. doi:10.1186/s12872-021-02048-9(IF:2.298)

重组生物素化人OX40/TNFRSF4/CD134蛋白(伯胺标记)(hFc标签) Human OX40/TNFRSF4/CD134 Protein

重组生物素化人OX40/TNFRSF4/CD134蛋白(伯胺标记)(hFc标签) Human OX40/TNFRSF4/CD134 Protein

产品说明书

FAQ

COA

已发表文献

 

性能参数

分子别名(Synonyms)

OX40L receptor;CD134; TNFRSF4; Ly-70

表达区间及表达系统(Source)

Biotinylated Human OX40/TNFRSF4/CD134 Protein (Primary Amine Labeling) is expressed from HEK293 with hFc tag at the C-Terminus. It contains Leu29-Ala216.[Accession | P43489]

分子量大小(Molecular Weight)

The protein has a predicted MW of 46.8 kDa. Due to glycosylation, the protein migrates to 72-75 kDa based on SDS-PAGE result.

内毒素(Endotoxin)

Less than 1EU per μg by the LAL method.

纯度(Purity)

> 95% as determined by SDS-PAGE

制剂(Formulation)

Supplied as 0.22μm filtered solution in PBS (pH 7.4).

 

储存条件

The product should be stored at -85~-65℃ for 1 year from date of receipt.

Recommend to aliquot the protein into smaller quantities when first used and avoid repeated freeze-thaw cycles.

 

注意事项

1.Please operate with lab coats and disposable gloves,for your safety.

2.This product is for research use only.

 

性能参数

分子别名(Synonyms)

OX40L receptor;CD134; TNFRSF4; Ly-70

表达区间及表达系统(Source)

Biotinylated Human OX40/TNFRSF4/CD134 Protein (Primary Amine Labeling) is expressed from HEK293 with hFc tag at the C-Terminus. It contains Leu29-Ala216.[Accession | P43489]

分子量大小(Molecular Weight)

The protein has a predicted MW of 46.8 kDa. Due to glycosylation, the protein migrates to 72-75 kDa based on SDS-PAGE result.

内毒素(Endotoxin)

Less than 1EU per μg by the LAL method.

纯度(Purity)

> 95% as determined by SDS-PAGE

制剂(Formulation)

Supplied as 0.22μm filtered solution in PBS (pH 7.4).

 

储存条件

The product should be stored at -85~-65℃ for 1 year from date of receipt.

Recommend to aliquot the protein into smaller quantities when first used and avoid repeated freeze-thaw cycles.

 

注意事项

1.Please operate with lab coats and disposable gloves,for your safety.

2.This product is for research use only.

人源高氧化程度低密度脂蛋白 Human High Ox-LDL|Human High Oxidized Low Density Lipoprotein(Human High Ox-LDL)

人源高氧化程度低密度脂蛋白 Human High Ox-LDL|Human High Oxidized Low Density Lipoprotein(Human High Ox-LDL)

产品说明书

FAQ

COA

已发表文献

产品描述

LDL是由极低密度脂蛋白(VLDL)转变而来,主要功能是把胆固醇运输到全身各处细胞,运输到肝脏合成胆酸,其可用于研究受体介导的内吞作用过程,尤其是在动脉粥样硬化等疾病中,其血浆来源的LDL可用于研究LDL在功能和代谢中的氧化作用。

氧化的LDLOx-LDL)是修饰LDL中的一类。修饰的LDL除包括氧化修饰的LDL外,还包括乙酰化LDL及丙二醛(MDA)、4-羟烯酸(4-HNE)直接结合的LDL,这些未经氧化修饰而仅经一般化学修饰的LDL称为衍化的LDL

不同于衍化的LDLOx-LDL 的生理学独特性表现在:

1)在细胞生理功能影响上,Ox-LDL可诱发细胞毒性作用,影响花生四烯酸的代谢,抑制胆固醇酯化作用等,但衍化的LDL无上述效应;

2Ox-LDL消耗LDL内源性抗氧化物质,使LDL上的维生素E含量下降,而MDA-LDL无上述效应;

3)氧化修饰涉及脂质过氧化反应,LDL中的PUFAs被氧化。MDALDL修饰,是直接和ApoB-100结合成希夫氏碱,脂质过氧化反应轻微;

4)氧化LDL在氧化程度低时,ApoB降解;在氧化程度高时,ApoB又可发生再聚合。MDALDL的修饰,ApoB无降解、聚合反应发生;

5Ox-LDL 产生的荧光峰波长为430nm,而MDA -LDL的荧光峰波长为460nmOx-LDL不经LDL受体代谢,由清道夫受体识别、结合、内吞饮入细胞并丧失正常的胆固醇代谢途径,引起细胞内脂质沉积,泡沫样变。

 

LDL氧化修饰的方式有很多种,常见的有:

1)细胞介导的LDL氧化修饰,又称为生物氧化修饰的LDL。如内皮细胞,巨噬细胞,单核细胞都具有此功能;

2)过度金属离子介导的LDL氧化修饰,如Ca2+Fe2+等;还有其他形式的氧化修饰,包括物理方法如紫外线,或过氧化物酶催化。

YEASEN提供的人源氧化低密度脂蛋白(Human High Oxidized Low Density LipoproteinHigh Ox-LDL),是由过度铜离子介导人血浆来源的LDL进行的氧化修饰。新鲜血浆经检测为HCVHBsAgHIV阴性。本产品为无菌包装,可以直接稀释使用。High Ox-LDL具有的高氧化水平使其产生明显的氧化应激,能够用来诱导细胞凋亡,以及建立细胞损伤模型。我们还提供中等氧化程度的Ox-LDL(货号:20605JP05),广泛用于脂质代谢的研究。除提供Ox-LDL,我们还提供人源乙酰化LDLAc-LDL,以及荧光标记的LDL 

 

制备方法

37℃Cu2SO4PBS溶液中氧化人LDL,加入过量的EDTA终止氧化反应。

 

产品性质

蛋白纯度(Purity

97%(琼脂糖凝胶电泳)

蛋白浓度Concentration

0.8-3.0 mg/ml

外观Appearance

无色乳状液体

缓冲液组分(Buffer Components

PBS, pH 7.4

氧化程度(Oxidized Level

TBARS检测(根据MDA的含量反映LDL的氧化程度)

起始LDL0.1~0.5 nmol MDA/mg蛋白

Ox-LDL90~100 nmol MDA/mg蛋白

 

稀释方法

根据实验需要用PBS磷酸盐缓冲液或细胞培养液稀释即可。

 

运输与保存方法

冰袋运输4℃保存,建议避光,保存时间不要超过4周。千万不可冻存!!

 

注意事项

1) 本品的稀释工作液极不稳定,强烈建议根据单次需要用量,新鲜配制工作液;

2) 长期贮存可能会有沉淀析出,属于正常现象,低速离心2 min去除沉淀即可使用;

3) LDLLDL受体的结合需要Ca2+Mn2+的参与,过量EDTA的存在会抑制其结合;

4) 为了您的安全和健康,请穿实验服并戴一次性手套操作。

 

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Human DiI-Ac-LDL 红色荧光标记人源乙酰化低密度脂蛋白

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Human DiI-Ox-LDL 人源红色荧光标记氧化型低密度脂蛋白

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HB200423

 

Q:该产品长期保存会出现少量沉淀,还可以使用吗?

A:这是正常现象。低速离心 1 ~2min 去除沉淀物,即得到澄清液。

Q:该产品一定要现用现配?

A:由于稀释的工作液极不稳定,建议即用即配。

Q:该产品如何储存?

A4ºC 无菌避光,收到货后可稳定保存 6 周。但不可冻存。

Q:该产品可以在实验工作台中使用吗?

A:本品为无菌包装,建议在超净工作台中操作。

人源高氧化程度低密度脂蛋白 Human High Ox-LDL|Human High Oxidized Low Density Lipoprotein(Human High Ox-LDL)

暂无内容

产品描述

LDL是由极低密度脂蛋白(VLDL)转变而来,主要功能是把胆固醇运输到全身各处细胞,运输到肝脏合成胆酸,其可用于研究受体介导的内吞作用过程,尤其是在动脉粥样硬化等疾病中,其血浆来源的LDL可用于研究LDL在功能和代谢中的氧化作用。

氧化的LDLOx-LDL)是修饰LDL中的一类。修饰的LDL除包括氧化修饰的LDL外,还包括乙酰化LDL及丙二醛(MDA)、4-羟烯酸(4-HNE)直接结合的LDL,这些未经氧化修饰而仅经一般化学修饰的LDL称为衍化的LDL

不同于衍化的LDLOx-LDL 的生理学独特性表现在:

1)在细胞生理功能影响上,Ox-LDL可诱发细胞毒性作用,影响花生四烯酸的代谢,抑制胆固醇酯化作用等,但衍化的LDL无上述效应;

2Ox-LDL消耗LDL内源性抗氧化物质,使LDL上的维生素E含量下降,而MDA-LDL无上述效应;

3)氧化修饰涉及脂质过氧化反应,LDL中的PUFAs被氧化。MDALDL修饰,是直接和ApoB-100结合成希夫氏碱,脂质过氧化反应轻微;

4)氧化LDL在氧化程度低时,ApoB降解;在氧化程度高时,ApoB又可发生再聚合。MDALDL的修饰,ApoB无降解、聚合反应发生;

5Ox-LDL 产生的荧光峰波长为430nm,而MDA -LDL的荧光峰波长为460nmOx-LDL不经LDL受体代谢,由清道夫受体识别、结合、内吞饮入细胞并丧失正常的胆固醇代谢途径,引起细胞内脂质沉积,泡沫样变。

 

LDL氧化修饰的方式有很多种,常见的有:

1)细胞介导的LDL氧化修饰,又称为生物氧化修饰的LDL。如内皮细胞,巨噬细胞,单核细胞都具有此功能;

2)过度金属离子介导的LDL氧化修饰,如Ca2+Fe2+等;还有其他形式的氧化修饰,包括物理方法如紫外线,或过氧化物酶催化。

YEASEN提供的人源氧化低密度脂蛋白(Human High Oxidized Low Density LipoproteinHigh Ox-LDL),是由过度铜离子介导人血浆来源的LDL进行的氧化修饰。新鲜血浆经检测为HCVHBsAgHIV阴性。本产品为无菌包装,可以直接稀释使用。High Ox-LDL具有的高氧化水平使其产生明显的氧化应激,能够用来诱导细胞凋亡,以及建立细胞损伤模型。我们还提供中等氧化程度的Ox-LDL(货号:20605JP05),广泛用于脂质代谢的研究。除提供Ox-LDL,我们还提供人源乙酰化LDLAc-LDL,以及荧光标记的LDL 

 

制备方法

37℃Cu2SO4PBS溶液中氧化人LDL,加入过量的EDTA终止氧化反应。

 

产品性质

蛋白纯度(Purity

97%(琼脂糖凝胶电泳)

蛋白浓度Concentration

0.8-3.0 mg/ml

外观Appearance

无色乳状液体

缓冲液组分(Buffer Components

PBS, pH 7.4

氧化程度(Oxidized Level

TBARS检测(根据MDA的含量反映LDL的氧化程度)

起始LDL0.1~0.5 nmol MDA/mg蛋白

Ox-LDL90~100 nmol MDA/mg蛋白

 

稀释方法

根据实验需要用PBS磷酸盐缓冲液或细胞培养液稀释即可。

 

运输与保存方法

冰袋运输4℃保存,建议避光,保存时间不要超过4周。千万不可冻存!!

 

注意事项

1) 本品的稀释工作液极不稳定,强烈建议根据单次需要用量,新鲜配制工作液;

2) 长期贮存可能会有沉淀析出,属于正常现象,低速离心2 min去除沉淀即可使用;

3) LDLLDL受体的结合需要Ca2+Mn2+的参与,过量EDTA的存在会抑制其结合;

4) 为了您的安全和健康,请穿实验服并戴一次性手套操作。

 

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20605JP05

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20606JP75

Human DiI-Ac-LDL 红色荧光标记人源乙酰化低密度脂蛋白

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Q:该产品长期保存会出现少量沉淀,还可以使用吗?

A:这是正常现象。低速离心 1 ~2min 去除沉淀物,即得到澄清液。

Q:该产品一定要现用现配?

A:由于稀释的工作液极不稳定,建议即用即配。

Q:该产品如何储存?

A4ºC 无菌避光,收到货后可稳定保存 6 周。但不可冻存。

Q:该产品可以在实验工作台中使用吗?

A:本品为无菌包装,建议在超净工作台中操作。

人源高氧化程度低密度脂蛋白 Human High Ox-LDL|Human High Oxidized Low Density Lipoprotein(Human High Ox-LDL)

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