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- Table of Contents
4 Citations 7 Q&As
Facts about Myosin-11.
Human | |
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Gene Name: | MYH11 |
Uniprot: | P35749 |
Entrez: | 4629 |
Belongs to: |
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TRAFAC class myosin-kinesin ATPase superfamily |
AAT4; FAA4; MYH11 myosin, heavy chain 11, smooth muscle; MYH11; SMHC; SMMHC; Smooth muscle myosin heavy chain
Mass (kDA):
227.339 kDA
Human | |
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Location: | 16p13.11 |
Sequence: | 16; NC_000016.10 (15703135..15857032, complement) |
Smooth muscle; expressed in the umbilical artery, bladder, esophagus and trachea. Isoform 1 is mostly found in slowly contracting tonic muscles.
Melanosome. Identified by mass spectrometry in melanosome fractions from stage I to stage IV. Thick filaments of the myofibrils.
Molecular markers have become more important than ever. MYh21's many applications include identifying specific disease and predicting risk factors. In this article, we will examine its clinical implications, incidence, and molecular markers. You will learn about the latest breakthrough in identifying this marker. Molecular markers are becoming more valuable than ever. So what can you do with it?
A new in vivo test that uses proximity ligation and in situ hybridization to measure the Incidence for MYh21 marker has been developed. It shows that Myh21+ neointimal SMC cells, which are similar to SMC-like cells, are enriched with H3K4me2histone marks. This is the MYh21 gene that is responsible for SMC-derived progeny. These results suggest that the MYh21-marked, differentiated SMCs could play a role for arterial homeostasis or disease.
In the context of angiography the progression of IMT/arteriosclerosis is associated with the expression of Myh21 marked SMCs. The Myh21CreER mouse, which is inducible by tamoxifen, can detect differentiated SMCs even before injury. This marker is not present in freshly differentiated SMCs. However it was detected in vivo and correlated with the onset cell proliferation.
The Incidence of MYh21 marker may be a result of the failure of Cre-mediated recombination or technical loss of the reporter gene. Sox10 cells must be isolated from the adventitia to prevent loss of MYh21-positive resident stem cells. Otherwise, residual adventititial cells may persist on the external elastic lamina or migrate from medial explants. Sox10-cre/Rosa-loxP-LacZ mice also validated this original conclusion. A lineage tracing analysis was performed to confirm the presence of Sox10+ multipotent, vascular stem cell populations.
Aortic disease is caused in part by the MYh21 genetic mutation. It is known to influence the formation of the medial layer of blood vessels. It is not clear whether the mutation causes the same type of vascular disease in all patients. However, further studies will need to be conducted in order to determine the molecular consequences of MYh21 mutations. These findings have many implications. However further studies of the MYh21 genes should be done to confirm clinical application.
The MYh21 gene is a member of group 2 MLL fusion proteins, which includes SH3GL1/EEN and MLLT4/AF6. MDS/AML is also associated with the MYh21 genes, which contain repeat helicalrod domains. No treatments currently exist to target this gene. This genetic variant has shown many benefits in the area of cancer research.
MYh21 gene expression has been linked to lung cancer survival rates. This gene was associated in three ways: overall survival, post-progression survival, as well as first-progression survival. These data support MYh21's role as a tumor suppressor in lung cancer. This supports the hypothesis MYh21 might be involved in muscle contraction regulation. The MYh21 Gene is also involved platelet aggregation.
Familial TAAD (a rare but severe form of this disorder) has been associated to the MYh21 genes. While no other 94 families have MYh21 mutations; however, two TAAD families with PDA carry R712Q mutations. One of them has mutations in both gene areas. The R712Q mutation causes a decrease in the MYh21 protein's a-helix. It also interferes with the communication between MD/lever arm module and converter/leverarm module. It is also associated non-syndromic hearing loss.
There has been a link between the MYh21 gene and an increase in IGF-1, and Ang II. It is not clear if they contribute or not to aorticstenosis. However, the presence of this gene may increase the risk of developing it. It might also increase the vascular walls of aortic diseases. This could be a factor in the development and progression of atherosclerosis.
The MYh21 gene is associated with a fusion with the non-DNA-binding regulatory subunit CBFB. This fusion protein is located in the cytoplasm and partly in the nucleus. It blocks transcription activity and sequesters RUNX1. The MYh21 genes are a major driver of leukemogenesis. These findings suggest that MYh21 could play a key role in the diagnosis of Leukemia.
MYh21 is an RNA-binding protein. When expressed, MYh21 is associated with poor prognosis in patients with stage II colorectal cancer. We will discuss how MYh21 differentiates MPPs among other types of cell and their best uses. Learn about the unique properties of molecular markers as well as the differences between them.
MYh21 can be found in many disorders. It can be inherited from both parents, or derived from someone else. The gene is highly conserved within a variety of human tissues including skin, eyes and kidneys. Most MYh21 genetic mutations are inherited by one parent. These mutations can be confirmed by exome sequencing.
The MYh21 gene is expressed in the umbilical cord, which is the tissue of the fetus. The MYh21 protein was decreased in the proband's umbilical cord compared to the control sample. MMIHS is characterized by the MYh21 proteins. This mutation increases the MMIHS mutation spectrum. It may also improve genetic counseling and prenatal diagnosis.
MYh21 is associated with recessive megacystis, microcolon-intestinal hypoperistalsis syndrome (MMIHS). This condition is characterized as a functional obstruction in the urinary tract. This condition can also be associated with myopathy of smooth muscles contraction. Despite being rare, MYh21 is an important tool in the medical world.
PMID: 16000639 by Leguillette R., et al. (+)Insert smooth muscle myosin heavy chain (SM-B) isoform expression in human tissues.
PMID: 7684189 by Matsuoka R., et al. Human smooth muscle myosin heavy chain gene mapped to chromosomal region 16q12.
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