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MABT535

Sigma-Aldrich

Anti-Desmin Antibody, clone 4C12.1

clone 4C12.1, from mouse

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.43

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

4C12.1, monoclonal

species reactivity

mouse, rat, human

packaging

antibody small pack of 25 μg

technique(s)

immunohistochemistry: suitable (paraffin)
western blot: suitable

isotype

IgG2bκ

NCBI accession no.

UniProt accession no.

shipped in

ambient

target post-translational modification

unmodified

Gene Information

human ... DES(1674)

General description

Desmin (UniProt: P17661) is encoded by the DES gene (Gene ID: 1674) in human. Desmin is a major class III intermediate filament protein essential for the structural integrity and function of muscle.
In adult striated muscle desmin forms a fibrous network connecting myofibrils to each other and to the plasma membrane from the periphery of the Z-line structures. It may also act as a sarcomeric microtubule-anchoring protein and specifically associate with detyrosinated tubulin-alpha chains, leading to buckled microtubules and mechanical resistance to contraction. Desmin is particularly abundant at the myotendinous junctions and at the neuromuscular junctions of skeletal muscle. Mammalian cardiac muscle cells contain higher amounts of desmin (up to 2% of total protein) compared to skeletal muscle cells (0.35% of total protein). Mutations in DES gene have been linked to familial cardiac and skeletal myopathy characterized by skeletal muscle weakness associated with cardiac conduction blocks, arrhythmias, and restrictive heart failure. It can also lead to myofibrillar destruction with intracytoplasmic accumulation of desmin-reactive deposits in cardiac and skeletal muscle cells. (rEF.: Denise Paulin, D., and Li, Z (2004). Experimental Cell Research 301(1); 1 -7).

Specificity

Clone 4C12.1 specifically detects Desmin in human, mouse, and rat muscles. It targets an epitope within 64 amino acids from the C-terminal end.

Immunogen

GST/His-taged recombinant fragment corresponding to 64 amino acids from the C-terminal region of human Desmin.

Application

Anti-Desmin Antibody, clone 4C12.1, Cat. No. MABT535, is a mouse monoclonal antibody that targets Desmin in Human, Mouse, and Rat and it is tested for use in Immunohistochemistry (Paraffin) and Western Blotting.
Immunohistochemistry Analysis: A 1:50 dilution from a representative lot detected Desmin in mouse heart, mouse skeletal muscle, rat heart, and rat skeletal muscle tissues.

Immunohistochemistry Analysis: A 1:1,000 dilution from a representative lot detected Desmin in human heart and human skeletal muscle tissues.
Research Category
Cell Structure

Quality

Evaluated by Western Blotting in human skeletal muscle tissue lysate.

Western Blotting Analysis: 0.5 µg/mL of this antibody detected Desmin in 10 µg of human skeletal muscle tissue lysate.

Target description

~53 kDa observed; 53.53 kDa calculated. Uncharacterized bands may be observed in some lysate(s).

Physical form

Format: Purified
Protein G purified
Purified mouse monoclonal antibody IgG2b in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Other Notes

Concentration: Please refer to lot specific datasheet.

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

12 - Non Combustible Liquids

wgk_germany

WGK 1


Certificates of Analysis (COA)

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Daniella Corporan et al.
Frontiers in cardiovascular medicine, 8, 714774-714774 (2021-11-05)
Introduction: Mitral regurgitation (MR) imposes volume overload on the left ventricle (LV) and elevates wall stress, triggering its adverse remodeling. Pronounced LV dilation, minimal wall thinning, and a gradual decline in cardiac ejection fraction (EF) are observed. The structural changes

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