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Rabbit Polyclonal Anti-TTN antibody (STJ98821)
Supplier: St John’s Laboratory Ltd.
Recommended applications: IHC-P, ELISA
Recommended dilution: IHC-P 1:50-300; ELISA 1:5000-20000
Recommended protocols: check protocols
Click or hover above images to see image description for Anti-TTN antibody.
Check alternative names for the antibodyExpand
SCBT cat No:
|Catalogue No.|| |
Human, Mouse, Rat
Anti-TTN antibody detects endogenous TTN.
Synthetic peptide from human protein at AA range: 161-210.
|Recommended dilution|| |
IHC-P 1:50-300; ELISA 1:5000-20000
Anti-TTN antibody was tube-contained in PBS, pH 7.4, containing 0.02% sodium azide as Preservative and 50% Glycerol.
Anti-TTN antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Database links|| |
|Protein function|| |
Key component in the assembly and functioning of vertebrate striated muscles. By providing connections at the level of individual microfilaments, it contributes to the fine balance of forces between the two halves of the sarcomere. The size and extensibility of the cross-links are the main determinants of sarcomere extensibility properties of muscle. In non-muscle cells, seems to play a role in chromosome condensation and chromosome segregation during mitosis. Might link the lamina network to chromatin or nuclear actin, or both during interphase. .
|Protein tissue specificity|| |
Isoforms 3, 7 and 8 are expressed in cardiac muscle. Isoform 4 is expressed in vertebrate skeletal muscle. Isoform 6 is expressed in skeletal muscle (at protein level). .
|Involvement in disease|| |
Hereditary myopathy with early respiratory failure (HMERF) [MIM:603689]: Autosomal dominant, adult-onset myopathy with early respiratory muscle involvement. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Cardiomyopathy, familial hypertrophic 9 (CMH9) [MIM:613765]: A hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Cardiomyopathy, dilated 1G (CMD1G) [MIM:604145]: 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.; Tardive tibial muscular dystrophy (TMD) [MIM:600334]: Autosomal dominant, late-onset distal myopathy. Muscle weakness and atrophy are usually confined to the anterior compartment of the lower leg, in particular the tibialis anterior muscle. Clinical symptoms usually occur at age 35-45 years or much later. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Limb-girdle muscular dystrophy 2J (LGMD2J) [MIM:608807]: An autosomal recessive degenerative myopathy characterized by progressive weakness of the pelvic and shoulder girdle muscles. Severe disability is observed within 20 years of onset. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Early-onset myopathy with fatal cardiomyopathy (EOMFC) [MIM:611705]: Early-onset myopathies are inherited muscle disorders that manifest typically from birth or infancy with hypotonia, muscle weakness, and delayed motor development. EOMFC is a titinopathy that, in contrast with the previously described examples, involves both heart and skeletal muscle, has a congenital onset, and is purely recessive. This phenotype is due to homozygous out-of-frame TTN deletions, which lead to a total absence of titin’s C-terminal end from striated muscles and to secondary CAPN3 depletion. . Note=The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. ; Contains 132 fibronectin type-III domains. ; Contains 152 Ig-like (immunoglobulin-like) domains. ; Contains 1 protein kinase domain. ZIS1 and ZIS5 regions contain multiple SPXR consensus sites for ERK- and CDK-like protein kinases as well as multiple SP motifs. ZIS1 could adopt a closed conformation which would block the TCAP-binding site.; The PEVK region may serve as an entropic spring of a chain of structural folds and may also be an interaction site to other myofilament proteins to form interfilament connectivity in the sarcomere.
|Protein post-translational modifications|| |
|Protein cellular localization|| |
Cytoplasm . Nucleus .
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St John’s Laboratory Ltd.
|Product type|| |
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