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MAB1950

Sigma-Aldrich

Anti-Integrin α2 Antibody, clone P1E6

clone P1E6, Chemicon®, from mouse

Synonym(s):

CD49b

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About This Item

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

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

P1E6, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable

isotype

IgG1

suitability

not suitable for immunohistochemistry (Paraffin)

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... ITGA2(3673)

Specificity

Reacts with Human a2 integrin.

Application

Anti-Integrin α2 Antibody, clone P1E6 is an antibody against Integrin α2 for use in IC, IH.
Research Category
Cell Structure
Research Sub Category
Integrins
Suitable for use in attachment inhibition assays using fibroblasts, epithelial cells, endothelial cells, and non-activated platelets on collagen types I, III, IV, VI and laminin.

Suitable for immunofluorescence using fresh frozen or acetone fixed tissues. Not recommended for traditional formalin fixed paraffin embedded tissues.

Final working dilutions must be determined by end user.

Physical form

Format: Purified
Protein A Purified mouse immunoglobulin in 0.01 M phosphate buffered saline, pH 7.1, with 0.1% sodium azide as a preservative.
Protein A purified

Storage and Stability

Maintain for 1 year at 2–8°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.

Analysis Note

Control
Skin (Basement membrane)

Other Notes

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

Legal Information

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

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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wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Hirokazu Date et al.
Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 28(2), 225-231 (2009-09-03)
Cellular activities responding to growth factors are important in ligament healing. The anterior cruciate ligament (ACL) has poor healing potential compared to the medial collateral ligament (MCL). To assess the differences, we investigated the proliferation, migration, adhesion, and matrix synthesis
Internalization of echovirus 1 in caveolae.
Marjomaki, V; Pietiainen, V; Matilainen, H; Upla, P; Ivaska, J; Nissinen, L; Reunanen et al.
Journal of virology null
N Théret et al.
Hepatology (Baltimore, Md.), 30(2), 462-468 (1999-07-27)
Fibrosis occurs in most chronic liver injuries and results from changes in the balance between synthesis and degradation of extracellular matrix components. In fibrotic livers, there is a markedly increased activity of matrix metalloproteinase 2 (MMP2), a major enzyme involved
Identification of P2Y12-dependent and -independent mechanisms of glycoprotein VI-mediated Rap1 activation in platelets.
Larson, MK; Chen, H; Kahn, ML; Taylor, AM; Fabre, JE; Mortensen, RM; Conley, PB; Parise, LV
Blood null
P D Arora et al.
The American journal of pathology, 154(3), 871-882 (1999-03-18)
Wound contraction is mediated by myofibroblasts, specialized fibroblasts that appear in large numbers as the wound matures and when resistance to contractile forces increases. We considered that the regulation of myofibroblast differentiation by wound-healing cytokines may be dependent on the

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