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Mouse Monoclonal Desmin antibody [10H7D2] (STJ97999)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:200-1:1000; ELISA 1:10000
Recommended protocols: check protocols
Click or hover above images to see image description for Desmin Monoclonal Antibody.
Check alternative names for the antibodyExpand
DES antibody,|CMD1I antibody|CSM1 antibody|CSM2 antibody|DES antibody|DESM_HUMAN antibody|Desmin antibody|FLJ12025 antibody|FLJ39719 antibody|FLJ41013 antibody|FLJ41793 antibody|Intermediate filament protein antibody|OTTHUMP00000064865 antibody|Anti-Desmin antibody [Y66] – Cytoskeleton Marker (ab32362)
SCBT cat No: sc-65983|sc-70961|sc-34200|sc-365130|sc-271677|sc-58744|sc-14026|sc-23879|sc-7559|
Desmin Monoclonal Antibody
|Catalogue No.|| |
Desmin Monoclonal Antibody detects endogenous levels of Desmin protein.
Purified recombinant fragment of Desmin expressed in E Coli
WB, IHC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:200-1:1000; ELISA 1:10000
Desmin Antibody was tube-contained. Purified antibody in PBS containing 0.03% sodium azide.
Desmin Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
|Protein names|| |
|Protein function|| |
Desmin are class-III intermediate filaments found in muscle cells. In adult striated muscle they form a fibrous network connecting myofibrils to each other and to the plasma membrane from the periphery of the Z-line structures .
|Involvement in disease|| |
Myopathy, myofibrillar, 1 (MFM1) [MIM:601419]: A neuromuscular disorder characterized by skeletal muscle weakness associated with cardiac conduction blocks, arrhythmias, restrictive heart failure, and by myofibrillar destruction with intracytoplasmic accumulation of desmin-reactive deposits in cardiac and skeletal muscle cells. . Note: The disease is caused by mutations affecting the gene represented in this entry. Mutations in the DES gene are associated with a variable clinical phenotype which encompasses isolated myopathies, pure cardiac phenotypes (including dilated cardiomyopathy, restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy), cardiac conduction disease, and combinations of these disorders. If both cardiologic and neurologic features occur, they can manifest in any order, as cardiologic features can precede, occur simultaneously with, or follow manifestation of generalized neuromuscular disease (PubMed:19879535). .; Cardiomyopathy, dilated 1I (CMD1I) [MIM:604765]: A disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Neurogenic scapuloperoneal syndrome Kaeser type (Kaeser syndrome) [MIM:181400]: Autosomal dominant disorder with a peculiar scapuloperoneal distribution of weakness and atrophy. A large clinical variability is observed ranging from scapuloperoneal, limb grindle and distal phenotypes with variable cardiac or respiratory involvement. Facial weakness, dysphagia and gynaecomastia are frequent additional symptoms. Affected men seemingly bear a higher risk of sudden, cardiac death as compared to affected women. Histological and immunohistochemical examination of muscle biopsy specimens reveal a wide spectrum of findings ranging from near normal or unspecific pathology to typical, myofibrillar changes with accumulation of desmin. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Limb-girdle muscular dystrophy 2R (LGMD2R) [MIM:615325]: A form of limb-girdle muscular dystrophy, a disease characterized by proximal weakness, weakness of the hip and shoulder girdles and prominent asymmetrical quadriceps femoris and biceps brachii atrophy. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the intermediate filament family.
|Protein post-translational modifications|| |
ADP-ribosylation prevents ability to form intermediate filaments.
|Protein cellular localization|| |
Cytoplasm > myofibril > sarcomere > Z line / Cytoplasm / Cell membrane > sarcolemma
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St John’s Laboratory Ltd.
|Product type|| |
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