M9570
Anti-Matrix Metalloproteinase-9 antibody produced in goat
affinity isolated antibody
Synonym(s):
MMP-9 Antibody - Anti-Matrix Metalloproteinase-9 antibody produced in goat, Mmp-9 Antibody, Anti-MMP-9
biological source
goat
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
species reactivity
mouse
technique(s)
immunohistochemistry: 5-15 μg/mL using cells or tissues
immunoprecipitation (IP): 25 μg/mL using conditioned media of transfected NSO cells
western blot: 0.25 μg/mL
UniProt accession no.
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
mouse ... Mmp9(17395)
General description
Matrix Metalloproteinase-9 encodes an enzyme that degrades type IV and V collagens.
Matrix metalloproteinase-9 (MMP-9) is a pro-inflammatory, zinc-dependent proteinase which is also known as 92kDa gelatinase. It is produced by various cells like granulocytes and mononuclear cells. The gene encoding it is localized on human chromosome 20q11.2-q13.1.
Immunogen
purified, NSO-derived, recombinant mouse matrix metalloproteinase-9.
Application
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunohistochemistry (1 paper)
Western Blotting (1 paper)
Immunohistochemistry (1 paper)
Western Blotting (1 paper)
Biochem/physiol Actions
Matrix metalloproteinase-9 (MMP-9) has been studied as a biomarker of nervous tissue inflammation in multiple sclerosis (MS).
This antibody recognizes pro and active mouse MMP-9. Immunoblotting and ELISA applications show an ~10% cross-reactivity with recombinant human MMP-9.
Physical form
Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline with 5% trehalose.
Disclaimer
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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Storage Class Code
11 - Combustible Solids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
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Cécile Cléry-Barraud et al.
Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI), 19(1), e146-e156 (2012-06-30)
To date, sulphur mustard (SM) cutaneous toxicity has been commonly assessed on account of several animal models such as pigs and weanling pigs. Few experiments however, have been carried out on mice so far. In this study, we aimed at
Nina Nguon et al.
Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society, 22(2), 272-280 (2014-03-19)
Data on the toxicity of lewisite (L), a vesicant chemical warfare agent, are scarce and conflicting, and the use of the specific antidote is not without drawbacks. This study was designed to evaluate if the SKH-1 hairless mouse model was
Yuta Morisaki et al.
Scientific reports, 6, 27354-27354 (2016-06-07)
Differential vulnerability among motor neuron (MN) subtypes is a fundamental feature of amyotrophic lateral sclerosis (ALS): fast-fatigable (FF) MNs are more vulnerable than fast fatigue-resistant (FR) or slow (S) MNs. The reason for this selective vulnerability remains enigmatic. We report
Hidemi Misawa et al.
Genesis (New York, N.Y. : 2000), 54(11), 568-572 (2016-09-07)
VAChT-Cre.Fast and VAChT-Cre.Slow mice selectively express Cre recombinase in approximately one half of postnatal somatic motor neurons. The mouse lines have been used in various studies with selective genetic modifications in adult motor neurons. In the present study, we crossed
Brigid K Jensen et al.
Glia, 70(7), 1426-1449 (2022-04-28)
Genetic mutations that cause amyotrophic lateral sclerosis (ALS), a progressively lethal motor neuron disease, are commonly found in ubiquitously expressed genes. In addition to direct defects within motor neurons, growing evidence suggests that dysfunction of non-neuronal cells is also an
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