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Key Documents

MAB3308

Sigma-Aldrich

Anti-MMP-2 Antibody, a.a. 468-483 hMMP2, clone 42-5D11

clone 42-5D11, Chemicon®, from mouse

Synonyme(s) :

Gelatinase A, 72 kDa Type IV Collagenase

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified antibody

Type de produit anticorps

primary antibodies

Clone

42-5D11, monoclonal

Espèces réactives

rat, bovine, human, rabbit, horse, mouse, pig

Fabricant/nom de marque

Chemicon®

Technique(s)

ELISA: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable

Isotype

IgG1κ

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... MMP2(4313)

Description générale

The matrix metalloproteinases (MMPs) are a family of at least eighteen secreted and membrane-bound zinc endopeptidases. Collectively, these enzymes can degrade all the components of the extracellular matrix, including fibrillar and non-fibrillar collagens, fibronectin, laminin and basement membrane glycoproteins. All MMPs are synthesized as proenzymes, and most of them are secreted from the cells as proenzymes. Thus, the activation of these proenzymes is a critical step that leads to extracellular matrix breakdown. MMPs are considered to play an important role in wound healing, apoptosis, bone elongation, embryo development, uterine involution, angiogenesis and tissue remodeling, and in diseases such as multiple sclerosis, Alzheimer′s, malignant gliomas, lupus, arthritis, periodontis, glumerulonephritis, atherosclerosis, tissue ulceration, and in cancer cell invasion and metastasis.
MMP2, also known as Gelatinase A, is a type IV collagenase that specifically cleaves type IV collagen, the major structural component of basement membranes. The metastatic potential of tumor cells has been found to correlate with the activity of this enzyme.

Spécificité

Specifically reacts with precursor and active forms of human MMP-2. Does not cross react with human MMP-1, -3, -9, or -13. Also reacts with rat, mouse, and bovine MMP2, other species not tested.

Immunogène

Epitope: a.a. 468-483 hMMP2
Synthetic oligopeptide corresponding to amino acid residue 468-483 (VTPRDKPMGPLLVATF) of human matrix metalloproteinase 2 (human MMP-2, gelatinase A).

Application

Immunoblotting 1-5 μg/mL

Immunohistochemistry on frozen and paraffin-embedded tissues using PLP fixation: 1-5 μg/mL (has not been tested in traditional formalin fixed tissues)

ElA
Research Category
Cell Structure
Research Sub Category
MMPs & TIMPs
This Anti-MMP-2 Antibody, a.a. 468-483 hMMP2, clone 42-5D11 is validated for use in ELISA, IH(P), WB for the detection of MMP-2.

Description de la cible

72 kDa

Forme physique

Format: Purified
Liquid in 0.1 M sodium phosphate buffer, pH 7.0 containing 2% protease free bovine Serum albumin.
Protein A purified

Stockage et stabilité

Maintain for 1 year at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Remarque sur l'analyse

Control
Lung, nerve, and various soft tissue tumors

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informations légales

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

Manufactured by Daiichi Fine Chemical Co., Ltd

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Xiaohu Fan et al.
American journal of physiology. Heart and circulatory physiology, 311(1), H183-H189 (2016-05-21)
Cardiomyocyte dedifferentiation may be an important source of proliferating cardiomyocytes facilitating cardiac repair. Cardiomyocyte dedifferentiation and proliferation induced by oncostatin-M (OSM) is characterized by sarcomere degeneration. However, the mechanism underlying sarcomere degeneration remains unclear. We hypothesized that this process may
Hazem Akkad et al.
PloS one, 9(4), e92622-e92622 (2014-04-08)
Critical illness myopathy (CIM) is a debilitating common consequence of modern intensive care, characterized by severe muscle wasting, weakness and a decreased myosin/actin (M/A) ratio. Limb/trunk muscles are primarily affected by this myopathy while cranial nerve innervated muscles are spared
Hien Thi Vu et al.
BioMed research international, 2018, 5971080-5971080 (2018-09-19)
All-trans retinoic acid (ATRA) is an effective drug for the induction therapy of acute promyelocytic leukemia. However, the treatment is associated with adverse events such as retinoic acid syndrome (RAS) in some patients, whose histologic characteristics included organ infiltration by
S B A Cau et al.
British journal of pharmacology, 164(2), 372-381 (2011-03-26)
Mounting evidence implicates matrix metalloproteinase (MMP) in the vascular dysfunction and remodelling associated with hypertension. We tested the hypothesis that treatment with pyrrolidine dithiocarbamate (PDTC), which interferes with NF-κB-induced MMPs gene transcription, could exert antihypertensive effects, prevent MMP-2 and MMP-9
Aline Vuckovic et al.
PloS one, 8(7), e69210-e69210 (2013-07-11)
The mechanisms by which tracheal occlusion (TO) improves alveolarization in congenital diaphragmatic hernia (CDH) are incompletely understood. Therefore transcriptional and histological effects of TO on alveolarization were studied in the rabbit model for CDH. The question of the best normalization

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