特别提示:包括重组人血管非炎性分子2(Vanin-2)在内,本公司的所有产品仅可用于科研实验,严禁用于临床医疗及其他非科研用途!
产品名称:重组人血管非炎性分子2(Vanin-2)
英文名称:Recombinant Human Vascular Non-Inflammatory Molecule 2
产品货号:JN0667
产品规格:10μg|50μg|500μg|1mg
本品由我们的哺乳动物细胞表达系统制备而成,目的基因编码的Gln23-Ser492在C端含有His标签。
Vanin-2质量控制:>95%(还原性SDS-PAGE)
Vanin-2制剂:冻干品
Vanin-2保存:
冻干蛋白置于-20℃以下可长期保存,室温条件下可稳定保存3周。
复溶蛋白溶液可在4~7℃保存2~7天,可分装后置于-20℃保存三个月。
Vanin-2复溶:
打开试剂管前请先离心。
复溶浓度推荐大于100 μg/ml。
冻干蛋白请溶于ddH2O。
复溶后,请根据用量分装冻存,避免反复冻融。
关于Vanin-2:
Vascular Non-Inflammatory Molecule 2 (VNN2) is a member of the CN hydrolase family. The family includes secreted and membrane-associated proteins, a few of which have been reported to participate in hematopoietic cell trafficking. they possess pantetheinase activity, which may play a role in oxidative-stress response. VNN2 is a GPI-anchored cell surface molecule that plays a role in transendothelial migration of neutrophils. VNN2 involved in the thymus homing of bone marrow cells. In addition, VNN2 may regulate beta-2 integrin-mediated cell adhesion, migration and motility of neutrophil.
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名称:重组人趋化因子CXCL2(MIP-2)
货号:JN0298
规格:10μg|50μg|500μg|1mg
本品由我们的大肠杆菌表达系统制备,目的基因编码的Thr39-Asn107表达纯化而来。
CXCL2/MIP-2质量控制:>95%(还原性SDS-PAGE)。
CXCL2/MIP-2制剂:冻干品
CXCL2/MIP-2保存:
冻干蛋白可在-20℃长期保存,室温也可稳定保存3周。
复溶蛋白溶液可在4~7℃保存2~7天。
复溶后建议分装冻存在-20℃,可保存3个月,应避免反复冻融。
CXCL2/MIP-2复溶:
1、试剂开盖前请先离心。
2、复溶浓度应大于100 μg/ml.
3、冻干蛋白溶于ddH2O中
4、复溶后根据使用量分装保存,避免反复冻融。
关于CXCL2/MIP-2:
Chemokine Ligand 2 (CXCL2) is a small secreted cytokine which belo
ngs to the CXC chemokine family. It is secreted by mo
nocytes and macrophages and chemotactic for polymorpho
nuclear leukocytes and hematopoietic stem cells. CXCL2 mobilizes cells by interacting with a cell surface chemokine receptor called CXCR2. It has been known to regulate immune functions mainly by chemo-attracting neutrophils. It is produced by activated mo
nocytes and neutrophils and expressed at sites of inflammation. It is a hematoregulatory chemokine, which suppresses hematopoietic progenitor cell proliferation. It can be induced by receptor activator of NF-kappaB ligand, the osteoclast (OC) differentiation factor, through JNK and NF-kappaB signaling pathways in OC precursor cells. CXCL2 in turn enhanced the proliferation of OC precursor cells of bone marrow-derived macrophages (BMMs) through the activation of ERK. Knockdown of CXCL2 inhibited both the proliferation of and the ERK activation in BMMs. During osteoclastogenesis CXCL2 stimulated the adhesion and the migration of BMMs. CXCL2 is a novel therapeutic target for inflammatory bone destructive diseases.
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