MMP2 Antibody - #AF0577

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Product: MMP2 Antibody
Catalog: AF0577
Description: Rabbit polyclonal antibody to MMP2
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog
Mol.Wt.: 74kDa; 74kD(Calculated).
Uniprot: P08253
RRID: AB_2834154

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 100ul $280 In stock
 200ul $350 In stock

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MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
MMP2 Antibody detects endogenous levels of total MMP2.
RRID:
AB_2834154
Cite Format: Affinity Biosciences Cat# AF0577, RRID:AB_2834154.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

72 kDa gelatinase; 72kD type IV collagenase; CLG 4; CLG 4A; CLG4; CLG4A; Collagenase Type 4 alpha; Collagenase type IV A; Gelatinase A; Gelatinase alpha; Gelatinase neutrophil; Matrix metallopeptidase 2 gelatinase A 72kDa gelatinase 72kDa type IV collagenase; Matrix metalloproteinase 2 (gelatinase A, 72kDa gelatinase, 72kDa type IV collagenase); Matrix Metalloproteinase 2; Matrix metalloproteinase II; Matrix metalloproteinase-2; MMP 2; MMP II; MMP-2; MMP2; MMP2_HUMAN; MONA; Neutrophil gelatinase; PEX; TBE 1; TBE-1;

Immunogens

Immunogen:
Uniprot:

P08253(MMP2_HUMAN) >>Visit HPA database.

Gene(ID):
MMP2(4313)
Expression:
P08253 MMP2_HUMAN:

Produced by normal skin fibroblasts. PEX is expressed in a number of tumors including gliomas, breast and prostate.

Description:
MMP2 Ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, and atherosclerotic plaque rupture. As well as degrading extracellular matrix proteins, can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. Also cleaves KISS at a Gly-|-Leu bond. Appears to have a role in myocardial cell death pathways.
Sequence:
MEALMARGALTGPLRALCLLGCLLSHAAAAPSPIIKFPGDVAPKTDKELAVQYLNTFYGCPKESCNLFVLKDTLKKMQKFFGLPQTGDLDQNTIETMRKPRCGNPDVANYNFFPRKPKWDKNQITYRIIGYTPDLDPETVDDAFARAFQVWSDVTPLRFSRIHDGEADIMINFGRWEHGDGYPFDGKDGLLAHAFAPGTGVGGDSHFDDDELWTLGEGQVVRVKYGNADGEYCKFPFLFNGKEYNSCTDTGRSDGFLWCSTTYNFEKDGKYGFCPHEALFTMGGNAEGQPCKFPFRFQGTSYDSCTTEGRTDGYRWCGTTEDYDRDKKYGFCPETAMSTVGGNSEGAPCVFPFTFLGNKYESCTSAGRSDGKMWCATTANYDDDRKWGFCPDQGYSLFLVAAHEFGHAMGLEHSQDPGALMAPIYTYTKNFRLSQDDIKGIQELYGASPDIDLGTGPTPTLGPVTPEICKQDIVFDGIAQIRGEIFFFKDRFIWRTVTPRDKPMGPLLVATFWPELPEKIDAVYEAPQEEKAVFFAGNEYWIYSASTLERGYPKPLTSLGLPPDVQRVDAAFNWSKNKKTYIFAGDKFWRYNEVKKKMDPGFPKLIADAWNAIPDNLDAVVDLQGGGHSYFFKGAYYLKLENQSLKSVKFGSIKSDWLGC

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Rabbit
100
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P08253 As Substrate

Site PTM Type Enzyme
T11 Phosphorylation
S160 Phosphorylation P17252 (PRKCA)
S246 Phosphorylation
T250 Phosphorylation P17252 (PRKCA)
T261 Phosphorylation
Y360 Phosphorylation
S362 Phosphorylation
T364 Phosphorylation
S365 Phosphorylation P17252 (PRKCA)
S369 Phosphorylation
T377 Phosphorylation P17252 (PRKCA)
T378 Phosphorylation P17252 (PRKCA)

Research Backgrounds

Function:

Ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, and atherosclerotic plaque rupture. As well as degrading extracellular matrix proteins, can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. Also cleaves KISS at a Gly-|-Leu bond. Appears to have a role in myocardial cell death pathways. Contributes to myocardial oxidative stress by regulating the activity of GSK3beta. Cleaves GSK3beta in vitro. Involved in the formation of the fibrovascular tissues in association with MMP14.

PEX, the C-terminal non-catalytic fragment of MMP2, posseses anti-angiogenic and anti-tumor properties and inhibits cell migration and cell adhesion to FGF2 and vitronectin. Ligand for integrinv/beta3 on the surface of blood vessels.

Mediates the proteolysis of CHUK/IKKA and initiates a primary innate immune response by inducing mitochondrial-nuclear stress signaling with activation of the pro-inflammatory NF-kappaB, NFAT and IRF transcriptional pathways.

PTMs:

Phosphorylation on multiple sites modulates enzymatic activity. Phosphorylated by PKC in vitro.

The propeptide is processed by MMP14 (MT-MMP1) and MMP16 (MT-MMP3). Autocatalytic cleavage in the C-terminal produces the anti-angiogenic peptide, PEX. This processing appears to be facilitated by binding integrinv/beta3.

Subcellular Location:

Secreted>Extracellular space>Extracellular matrix. Membrane. Nucleus.
Note: Colocalizes with integrin alphaV/beta3 at the membrane surface in angiogenic blood vessels and melanomas. Found in mitochondria, along microfibrils, and in nuclei of cardiomyocytes.

Cytoplasm. Mitochondrion.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Produced by normal skin fibroblasts. PEX is expressed in a number of tumors including gliomas, breast and prostate.

Subunit Structure:

Interacts (via the C-terminal hemopexin-like domains-containing region) with the integrin alpha-V/beta-3; the interaction promotes vascular invasion in angiogenic vessels and melamoma cells. Interacts (via the C-terminal PEX domain) with TIMP2 (via the C-terminal); the interaction inhibits the degradation activity. Interacts with GSK3B.

Family&Domains:

The conserved cysteine present in the cysteine-switch motif binds the catalytic zinc ion, thus inhibiting the enzyme. The dissociation of the cysteine from the zinc ion upon the activation-peptide release activates the enzyme.

Belongs to the peptidase M10A family.

Research Fields

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Specific types > Bladder cancer.   (View pathway)

· Organismal Systems > Immune system > Leukocyte transendothelial migration.   (View pathway)

· Organismal Systems > Endocrine system > Estrogen signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). Phenytoin silver: a new nanocompound for promoting dermal wound healing via comprehensive pharmacological action. Theranostics, 2017 (PubMed: 28255340) [IF=12.4]

Application: WB    Species: human    Sample:

Figure 6. PnAg regulates gp130/Jak/Stat3 signaling pathway (A) and (B) NIH-3T3 and HaCat Cells were treated with PnAg at different concentrations and cell viability was tested using MTT analysis. (C) Wound healing assay reflected the effect of PnAg on cell migration. (D) Binding mode of PnAg in the active pocket of gp130. (E) and (F) MMPs activity and expression levels of Stat3, VEGF, TGFB-1, and TGFB1 detected using zymographic and Western blot assays. (G) Diagram of the proposed function of PnAg in wound inflammation and re-epithelialization controls.

Application: IHC    Species: human    Sample:

Figure 2. PnAg promotes wound healing in SD rats. (A) Photographs of rat skin full-thickness excision wounds on different post-excision days. (B) Change in wound areas of SD rats after treatment; (C) and (D) Expression levels of collagen I, NF-κB, TGF-ß, MMP-2, and MMP-9 in tissues on day 7 and 17 detected by immunohistochemistry. (E) Histogram of protein expression levels in these tissues. (F) and (G) Histomorphological changes in wound tissues stained by Masson trichrome and HE on day 17.
2). Echinatin inhibits the growth and metastasis of human osteosarcoma cells through Wnt/β-catenin and p38 signaling pathways. Pharmacological Research, 2023 (PubMed: 37023991) [IF=9.3]

Application: WB    Species: Human    Sample: OS cells

Fig. 4. Ecn inhibits the migration and invasion of OS cells. (A) The effect of Ecn on the migration of OS cells (Wound healing assay, 100 ×). (B) The effect of Ecn on the migration of OS cells (Transwell assay, 100 ×). (C) The effect of Ecn on the invasion of OS cells (Matrigel-coated Transwell assay, 100 ×). (D) The effect of Ecn on the protein level of MMP2, MMP7, MMP9, Snail, Vimentin, N-Cadherin and E-Cadherin in OS cells (Western blot). ##P 
3). Foxq1 promotes metastasis of nasopharyngeal carcinoma by inducing vasculogenic mimicry via the EGFR signaling pathway. Cell Death & Disease, 2021 (PubMed: 33875643) [IF=9.0]

Application: WB    Species: mouse    Sample: tumors

Fig. 5 |Foxq1 promotes VM formation, and NPC growth and metastasis through regulating EGFR in vivo.H Metastatic nodules by tail vein injection of each group and normal lung (left). Image of H&E staining of lung sections from each group (right); Scale bars represent 500 μm. I Statistical results of the metastatic nodules in each group; p < 0.001. The expression of related genes in xenograft tumors from each group were monitored by qRT-PCR (J)and western blot (K). Data are presented as mean ± SD of three independent experiments.

Application: IF/ICC    Species: mouse    Sample: 5–8F cells

Fig. 7| MiR-124 inhibits the EGFR signaling pathway and VM formation, that could be rescued by Foxq1 expression. E Immunofluorescence staining of Foxq1, EGFR, VE-cadherin, MMP2 and MMP9 in 5–8F cells that overexpressed miR-124, control or simultaneously Foxq1 and miR-124, respectively; scale bars represent 50μm. qRT-PCR (F) and western blot (G) were used to monitor the expression of EGFR signaling pathway and VM-related genes in 5–8F cells that overexpressed miR-124, control or simultaneously Foxq1 and miR-124, respectively.Data are presented as mean ± SD of three independent experiments.
4). RETRACTED ARTICLE: Hsp90β promotes aggressive vasculogenic mimicry via epithelial–mesenchymal transition in hepatocellular carcinoma. Oncogene, 2018 (PubMed: 30087438) [IF=8.0]
5). Hsp90β promotes aggressive vasculogenic mimicry via epithelial-mesenchymal transition in hepatocellular carcinoma. ONCOGENE, 2023 (PubMed: 30087438) [IF=8.0]

Application: WB    Species: human    Sample: PLC-PRF-5 cells

Fig. 5| Hsp90β promotes Twist1 nuclear translocation and binding to VE-cadherin promoter to increase VM-related gene networks. eWestern blot analysis of VM and EMT-related markers, including VE-cadherin, VEGFR1, VEGFR2, E-cadherin, Vimentin, MMP2, and MMP9 in PLC-PRF-5 cells overexpressed Hsp90β or under lack of Twist1.

Application: IHC    Species: human    Sample: tumor

Fig. 6 | Hsp90β promotes tumor growth and VM formation relied on Twist1 in vivo and Hsp90 inhibitor depresses the promotion effect.e, f Hsp90β, Twist1, VE-cadherin, E-cadherin, Vimentin,MMP2, and MMP9 expression levels were measured in tumor tissue of the control, Hsp90β overexpression, Hsp90β+ Twist1 siRNA,control shRNA, and Hsp90β knockdown groups by IHC.
6). Aiduqing formula suppresses breast cancer metastasis via inhibiting CXCL1-mediated autophagy. PHYTOMEDICINE, 2021 (PubMed: 34247114) [IF=7.9]

Application: WB    Species: Human    Sample: breast cancer cells

Fig. 1. ADQ formula suppresses autophagy and induces apoptosis of high-metastatic breast cancer cells. (A) The HPLC fingerprints of the five independent batches of ADQ formula samples as well as its major components including p-coumaric acid, calycosin-7-glucoside, liquiritin and glycyrrhizic acid and curcumol. The HPLC fingerprints of five independent batches of ADQ formula were similar to one another. (B) The Effects of ADQ formula on cell proliferation in both the nonmalignant mammary epithelial cells and the highly metastatic breast cancer cells. Colony formation assay for evaluating the long-term influence of ADQ formula on MDA-MB-231 and BT-549 cells. The results showed that ADQ formula remarkably inhibited the proliferation of the breast cancer cell lines MDA-MB-231 and BT549 in a time- and dose-dependent manner, while having no obvious cytotoxicity in non-malignant cell lines including MCF-10A, HBL100, and HSF. (C-D) Wound healing assay and transwell assay for evaluating the migration and invasion inhibitory effects of ADQ formula on MDA-MB-231 and BT-549 cells. The results indicated that ADQ formula significantly inhibited cellular migratory and invasive capacities of MDA-MB-231 and BT-549 cells. (E) The expression levels of metastasis-related proteins in MDA-MB-231 and BT-549 cells using western blotting analysis after treating with ADQ formula in a concentration-dependent manner. The results indicated that ADQ-formula treatment for 24 h dramatically attenuated the expression levels of proteins related to basement-membrane degradation and the EMT. All values are presented as the mean ± SD, n = 3, * p < 0.05, ** p < 0.01.
7). Myricetin suppresses the proliferation and migration of vascular smooth muscle cells and inhibits neointimal hyperplasia via suppressing TGFBR1 signaling pathways. PHYTOMEDICINE, 2021 (PubMed: 34500301) [IF=7.9]

Application: WB    Species: Human    Sample: VSMCs

Fig. 2. Myricetin suppresses migration of VSMCs. (A) Wound healing assay was employed to detect (A) HASMC and (B) A7R5 cell migration at 0 and 48 h after incubation with different doses of myricetin (15, 30 and 60 μM) for 24 h. Scale bars, 200 μm. (C, D) Migration ratio was calculated as follows: ( wound width at 0 h − wound width at 48 h)/wound width at 0 h × 100% (n = 3). (E) Transwell assay was used to detect the proliferative capability of VSMCs before incubation with myricetin (15, 30 and 60 μM) for 24 h. Scale bars, 100 μm. (F, G) Quantification of the Transwell assay (n = 5). (H) Western blotting was used to assess MMP-9 and MMP-2 expression in cells treated with different doses of myricetin for 24 h. (I-L) The densitometry analysis and quantitative results of (H) (n = 3). Data are displayed as mean ± standard deviation (SD). * p < 0.05, ** p < 0.01 compared with the control group.
8). Ischemic Preconditioning Alleviates Cerebral Ischemia-Reperfusion Injury by Interfering With Glycocalyx. Translational stroke research, 2023 (PubMed: 36168082) [IF=6.9]
9). Ischemic Preconditioning Alleviates Cerebral Ischemia–Reperfusion Injury by Interfering With Glycocalyx. Translational Stroke Research, 2022 (PubMed: 36168082) [IF=6.9]
10). MicroRNA-181a regulates epithelial-mesenchymal transition by targeting PTEN in drug-resistant lung adenocarcinoma cells. INTERNATIONAL JOURNAL OF ONCOLOGY, 2015 (PubMed: 26323677) [IF=5.2]

Application: WB    Species: human    Sample: A549 cells

Figure 3. A549/DDP and A549/PTX cells showed molecular and morphological changes that were consistent with EMT. (A) microscopy at x200 magnification was used to assess cell morphology. The A549 cells (parental cells) had an epithelioid, rounded cobblestone appearance and there was limited formation of pseudopodia. A549/PTX and A549/DDP cells exhibited a spindle-shaped morphology and an increased formation of pseudopodia, indicating a loss of cell polarity. (B) E-cadherin, β-catenin, vimentin, MMP-2 and MMP-9 which are EMT-related proteins, were assessed in terms of expression levels. EMT-related transcription factors (Snail, Slug, Twist and ZEB1) were measured in A549/PTX and A549/DDP cells using western blot analysis. (C) The expression changes were confirmed at the mRNA level by qRT-PCR. Expression was standardized to the expression of GAPDH and normalized to 1.0 in the parental cells (compared with the parental A549 cells, means ± SEM, n=3, * P<0.05)

Application: WB    Species: human    Sample: A549 cells

Figure 6. |Overexpression of miR-181a in A549 cells induces morphological and molecular changes characteristic of EMT. (A) Twenty-four hours after transfection, cell morphology was observed by microscopy at x200 magnification for non-transfected A549 cells (blank), A549 cells transfected with mimic-NC or miR-181a-mimic. (B) E-cadherin, β-catenin, vimentin, MMP-9, MMP-2, Snail, Slug, Twist and ZEB1 expression levels after transfection were determined by western blot analysis.
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