Rabbit Anti-MMP2 Polyclonal antibody (CPBT-55715RC)

Rabbit Anti-Human MMP2 Polyclonal antibody for WB, IP, IHC, IF, ELISA


Host Species
Antibody Isotype
Species Reactivity
Human, Mouse, Rat, Zebrafish, Rabbit


Application Notes
WB: 1:500-1:1000
IP: 0.5-4.0 ug for IP and 1:200-1:1000 for WB
IHC: 1:100-1:400
IF: 1:50-1:500
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
MMP2; matrix metallopeptidase 2 (gelatinase A, 72kDa gelatinase, 72kDa type IV collagenase); CLG4; MONA; CLG4A; MMP-2
Entrez Gene ID
UniProt ID


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Custom Antibody Labeling

We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket


Beneficial effects of genistein in suppression of proliferation, inhibition of metastasis, and induction of apoptosis in PC3 prostate cancer cells


Authors: Shafiee, Gholamreza; Saidijam, Massoud; Tayebinia, Heidar; Khodadadi, Iraj

Objectives: Beneficial effects of genistein have been studied in various cancer types but the underlying molecular mechanisms of its actions have not been well established. This study investigated the effects of genistein on caspase-3 and p38 mitogen-activated protein kinase (p38MAPK) as main cellular signalling targets in PC3 prostate cancer cells. Methods: Caspase-3 and p38MAPK gene expression and intracellular protein levels were determined. Matrix metalloproteinase-2 (MMP2) gelatinase activity and caspase-3 enzyme activity were measured and PC3 cell migration and proliferation potencies were assessed. Results: Genistein induced apoptosis by enhancing the gene expression, intracellular protein level, and enzyme activity of caspase-3. Genistein also inhibited cell proliferation by reducing p38MAPK gene expression and protein level and strongly suppressed metastatic potency of PC3 cells by reducing MMP2 activity. Conclusion: Genistein exhibits its beneficial anticancer properties on PC3 cells by reducing metastatic potency and regulating caspase-3 and p38MAPK pathways at different transcriptional and protein levels.

HOTTIP knockdown inhibits cell proliferation and migration via regulating miR-490-3p/HMGB1 axis and PI3K-AKT signaling pathway in ox-LDL-induced VSMCs


Authors: Guo, Xiaoyan; Liu, Yuhao; Zheng, Xiaohui; Han, Yan; Cheng, Jiangtao

Aims: Atherosclerosis (AS) is a common cardiovascular disease with complicated pathogenesis. Long non-coding RNAs (lncRNAs) have been reported to be associated with AS progression. We aimed to explore the role and underlying mechanism of HOXA transcript at the distal tip (HOTTIP) in AS. Materials and methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of HOTTIP, miR-490-3p and high mobility group B 1 (HMGB1) in AS patients' sera and oxidized low-density lipoprotein (ox-LDL) induced human aortic vascular smooth muscle cells (HA-VSMCs). Cell Counting Kit-8 (CCK-8) assay and transwell assay were conducted to evaluate the proliferation and migration of HA-VSMCs, respectively. Western blot assay was carried out to determine the levels of proliferating cell nuclear antigen (PCNA), matrix metalloprotein 2 (MMP2), MMP9 and HMGB1. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to verify the targeting association between HOTTIP and miR-4903p, as well as miR-490-3p and HMGB1. Key findings: HOTTIP and HMGB1 were upregulated and miR-490-3p was downregulated in the sera of AS patients and ox-LDL-stimulated HA-VSMCs. HOTTIP knockdown suppressed ox-LDL induced proliferation and migration in HA-VSMCs. MiR-490-3p was identified as a target of HOTTIP and HOTTIP overexpression abolished the inhibition on cell proliferation and migration mediated by miR-490-3p in ox-LDL-induced HA-VSMCs. Moreover, miR-490-3p inhibition promoted cell proliferation and migration by directly targeting HMGB1 in ox-LDL-induced HA-VSMCs. Besides, HOTTIP knockdown repressed the activation of PI3K-AKT signaling pathway. Significance: HOTTIP knockdown suppressed cell proliferation and migration by regulating miR-490-3p/HMGB1 axis and PI3K-AKT pathway in ox-LDL-induced HA-VSMCs.

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