SDF-1 alpha/CXCL12 蛋白, Mouse (68a.a, CHO)

SDF-1 alpha (Stromal Cell-Derived Factor-1α, SDF-1α) is a member of the chemokine α subfamily that lack the ELR domain. SDF-1α works as a chemoattractant for T- and B-lymphocytes and monocytes. SDF-1α is a ligand for CXCR4. The SDF-1α/CXCR4 signaling mediates many physiological processes including cell trafficking, angiogenesis, embryogenesis, tumor invasion and metastatic. It also controls the chemotaxis of hematopoietic stem cells homing to the bone marrow^[1][2]. SDF-1 alpha/CXCL12 Protein, Mouse (68a.a, CHO) is produced in CHO cells, and consists of 68 amino acids (K22-K89).

基质细胞衍生因子-1（SDF-1）是趋化因子家族的重要成员，有两种亚型：SDF-1α和SDF-1β，其中SDF-1α是主要亚型。SDF-1α广泛存在于人体的许多组织和器官中，如淋巴结、骨髓、肝、肺、肌肉、小肠、肾、脑等，并能在这些器官和组织中持续存在。研究表明，SDF-1α在多种细胞的迁移、分布、发育、分化、凋亡等生理功能中发挥着重要作用。而且，SDF-1α在炎症、肿瘤形成和转移、病原体感染、伤口修复等一些疾病的病理过程中发挥着关键作用^{[1][3].
SDF-1 具有 α、β 和 γ 三种亚型，它们在剪接水平上有所不同，而不是在转录水平上有所不同。对人和小鼠 SDF-1 基因组结构的分析揭示了两种亚型：SDF-1α 和 SDF-1β，它们由单个基因编码并由选择性剪接产生。SDF-1α包含3个外显子，编码89个氨基酸的蛋白质，而SDF-1β包含4个外显子，编码93个氨基酸的蛋白质。两种异构体的序列高度相似，唯一的区别是 SDF1β C 末端多了 4 个氨基酸。在成年大鼠大脑中，SDF-1α 是主要的一种，存在于星形胶质细胞、小胶质细胞以及神经元中。SDF-1α 在正常胆碱能神经元（例如内侧隔膜和无名质）和多巴胺能神经元（例如黑质（SN）致密部和腹侧被盖区）中呈阳性。SDF-1α 是 CXCR4 唯一已知的配体。CXCR4 也是人类免疫缺陷病毒 (HIV) 结合的靶点[1][2]。
使用缺血再灌注模型和模型进行体外和体内研究SDF-1α 预处理可通过激活 ERK-1/2 和 AKT 磷酸化来缩小梗塞面积并增强对缺氧损伤和细胞凋亡的抵抗力[1]。SDF-1α/CXCR4 信号传导通过与神经递质和神经肽系统、神经内分泌系统的相互作用维持中枢神经系统稳态[2]。越来越多的动物实验表明，SDF-1α可以增强BMSC的迁移能力，动员BMSC到病变部位，促进其增殖和分化[3]。}

Recombinant mouse SDF-1α (10 ng/mL or 30 ng/mL; for 6 days) promotes osteoclast differentiation and activity in bone marrow mononuclear cells (BMMCs). SDF-1α can promote osteoclast formation and the expression oftartrate resistant acid phosphatase (TRAP), cathepsin K (CK), and MMP-9 in osteoclasts by activating the MAPK pathway, including ERK and p38, but not JNK^[4].

In a mouse acute myocardial infarction (AMI) model, recombinant mouse SDF-1α (100 ng/50 μL) injected into the infarctregions of the myocardium 3 to 4 times per mouse. Two weeks after infarction, the myocardial recruitment of c-kit⁺ cells is significantly higher in the group treated with the SDF-1alpha PEGylated fibrin patch than in the AMI control group^[5].

The EC₅₀ is <1.5 μg/mL as measured on Ca²⁺ mobilization assay in CHO-K1/Gα15/mCXCR4 cells (human Gα15 and mCXCR4 stably expressed in CHO-K1 cells).

Mouse

CHO

Tag Free

P40224 (K22-K89)

20315  [NCBI]

KPVSLSYRCPCRFFESHIARANVKHLKILNTPNCALQIVARLKNNNRQVCIDPKLKWIQEYLEKALNK

Approximately 8 kDa

Greater than 95% as determined by reducing SDS-PAGE.

无菌粉末.

Lyophilized after extensive dialysis against PBS.

<0.2 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Santhosh K Ghadge, et al. SDF-1α as a therapeutic stem cell homing factor in myocardial infarction. Pharmacol Ther. 2011 Jan;129(1):97-108.  [Content Brief]

  [2]. Kryczek I, et al. Stroma-derived factor (SDF-1/CXCL12) and human tumor pathogenesis. Am J Physiol Cell Physiol. 2007 Mar;292(3):C987-95.  [Content Brief]

  [3]. Zheng Jiang, et al. Contribution of SDF-1α/CXCR4 signaling to brain development and glioma progression. Neurosignals. 2013;21(3-4):240-58.  [Content Brief]

  [4]. Zhiqiang Meng, et al. SDF Factor-1α Promotes the Migration, Proliferation, and Osteogenic Differentiation of Mouse Bone Marrow Mesenchymal Stem Cells Through the Wnt/β-Catenin Pathway. Stem Cells Dev. 2021 Jan 15;30(2):106-117.  [Content Brief]

  [5]. Yonghui Dong, et al. Inhibition of SDF-1α/CXCR4 Signalling in Subchondral Bone Attenuates Post-Traumatic Osteoarthritis. Int J Mol Sci. 2016 Jun 16;17(6):943.  [Content Brief]

  [6]. Ge Zhang, et al. Controlled release of stromal cell-derived factor-1 alpha in situ increases c-kit+ cell homing to the infarcted heart. Tissue Eng. 2007 Aug;13(8):2063-71.  [Content Brief]