DCIP-1/CXCL3 蛋白, Mouse (P.pastoris)

CXCL3 is a chemoattractant for neutrophils and belongs to CXC chemokine subfamily. CXCL3 is a secreted growth factor that signals through its cognate receptor CXCR2. CXCL3 is involved in many immune responses including wound healing, cancer metastasis, and angiogenesis^[1][2]. DCIP-1/CXCL3 Protein, Mouse (P.pastoris) is produced in P.pastoris , and consists of 73 amino acids (A28-S100).

CXCL3 也称为 MIP-2 beta，在小鼠中称为 DCIP-1，在大鼠中称为 CINC2，在人类中称为 GRO-gamma。CXCL3 是 CXC 趋化因子亚家族的成员，它被细分为 Glu-Leu-Arg (ELR+) CXC 趋化因子。CXCL3 最初是在培养的黑色素瘤细胞系的上清液中发现的，被称为 GRO（生长相关癌基因）^[1]。既往研究报道CXCL3由巨噬细胞、成骨细胞、气道上皮、树突状细胞、滑膜成纤维细胞和癌症产生^[2]。
人CXCL3蛋白的氨基酸序列同源性较低小鼠和大鼠CXCL3蛋白之间的差异。
CXCL3在白细胞趋化、血管生成、肿瘤发生和细胞侵袭中发挥重要作用。CXCL3通过激活CXCR2受体，通过p38 MAPK、ERK1/2 MAPK和JAK2/STAT3等多种信号通路发挥其功能。CXCL3 在多种肿瘤疾病中高表达，包括黑色素瘤、前列腺癌、结直肠癌、侵袭性乳腺癌、肝细胞癌 (HCC)，以及肝损伤和炎症期间^[3][4] 。
受 CXCL3（以及 CXCL1 和 CXCL2）作用影响的癌症类型包括前列腺癌、胰腺癌、黑色素瘤、肺癌、肝细胞癌和胃癌[1]< /sup>。CXCL3 通过脂肪细胞中自分泌/旁分泌方式诱导 c/ebpb 和 c/ebpd，从而促进脂肪形成[2]。此外，CXCL3 还与血管侵犯和肿瘤包膜形成相关^[3]。CXCL3 在哮喘严重程度和哮喘气道重塑中发挥作用^[5]。

Measured by its binding ability in a Ca2+ mobilization assay. The ED₅₀ value of mouse DCIP-1/CXCL3 on Ca2+ mobilization assay in CHO-K1/Ga15/mCXCR2 cells (human Ga15 and mouse CXCR2 stably expressed in CHO-K1 cells) is less than 100.0 ng/ml.

Mouse

P. pastoris

Tag Free

Q6W5C0 (A28-S100)

330122  [NCBI]

AVVASELRCQCLNTLPRVDFETIQSLTVTPPGPHCTQTEVIATLKDGQEVCLNPQGPRLQIIIKKILKSGKSS

Approximately 9 kDa

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

无菌粉末.

Lyophilized after extensive dialysis against PBS.

<1 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]. Niradiz Reyes, et al. CXCL3 Signaling in the Tumor Microenvironment. Adv Exp Med Biol. 2021;1302:15-24.  [Content Brief]

  [2]. Smith DF, et al. GRO family chemokines are specialized for monocyte arrest from flow. Am J Physiol Heart Circ Physiol. 2005 Nov;289(5):H1976-84.  [Content Brief]

  [3]. Joji Kusuyama, et al. CXCL3 positively regulates adipogenic differentiation. J Lipid Res. 2016 Oct;57(10):1806-1820.  [Content Brief]

  [4]. Farioli-Vecchioli S, et al. Tis21 knock-out enhances the frequency of medulloblastoma in Patched1 heterozygous mice by inhibiting the Cxcl3-dependent migration of cerebellar neurons.J Neurosci. 2012 Oct 31;32(44):15547-64.  [Content Brief]

  [5]. Khushboo Gulati, et al. Molecular cloning and biophysical characterization of CXCL3 chemokine. Int J Biol Macromol. 2018 Feb;107(Pt A):575-584.  [Content Brief]

  [6]. Jinru Weng, et al. CXCL3 overexpression affects the malignant behavior of oral squamous cell carcinoma cells via the MAPK signaling pathway. J Oral Pathol Med. 2021 Oct;50(9):902-910.  [Content Brief]

  [7]. Laila A Al-Alwan, et al. Differential roles of CXCL2 and CXCL3 and their receptors in regulating normal and asthmatic airway smooth muscle cell migration. J Immunol. 2013 Sep 1;191(5):2731-41.  [Content Brief]

  [8]. Manuela Ceccarelli, et al. Suppression of Medulloblastoma Lesions by Forced Migration of Preneoplastic Precursor Cells with Intracerebellar Administration of the Chemokine Cxcl3. Front Pharmacol. 2016 Dec 16;7:484.  [Content Brief]