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- Table of Contents
Facts about NAD-dependent protein deacetylase sirtuin-6.
Deacetylation of nucleosomes interferes with RELA binding to target DNA. May be needed for the institution of WRN with telomeres during S-phase and for normal telomere maintenance.
Mouse | |
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Gene Name: | Sirt6 |
Uniprot: | P59941 |
Entrez: | 50721 |
Belongs to: |
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sirtuin family |
EC 3.5.1.-; NAD-dependent deacetylase sirtuin-6; SIR2L6sir2-related protein type 6; SIR2-like protein 6; sirtuin (silent mating type information regulation 2 homolog) 6 (S. cerevisiae); sirtuin (silent mating type information regulation 2, S. cerevisiae, homolog) 6; sirtuin 6; sirtuin type 6
Mass (kDA):
36.92 kDA
Mouse | |
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Location: | 10 C1|10 39.72 cM |
Sequence: | 10; |
Highest levels are found in muscle, thymus, spleen, brain and heart (at protein level).
This article will review monoclonal antibodies to the anti-SIRT6 gene as well as the activator MDL-811. We will also discuss the benefits of PQQ and DNA repair. We will also review the Boster Bio SIRT6 Marker ELISA Kit. This kit can be used for both ELISA or IF applications.
If you're in search of an affordable, high-sensitivity, and highly specific antibody, Boster Bio offers the Anti-SIRT6 Monoclonal Antibody. This antibody reacts with Human and Mouse and has a shelf-life of 1 year or more when stored at -20 degrees Celsius. It can be utilized in ELISA, Flow Cytometry, and IHC assays.
In their study, Huang and colleagues discovered the discovery of a new, cellularly active SIRT6 allosteric activator. The new compound reduced inflammation in the brain and improved the symptoms of sickness in the neuroinflammatory mouse model induced by LPS. They also discovered that MDL-811 is able to activate SIRT6 in both neurons and cancerous cells. MDL-811 was identified as an excellent SIRT6 activator.
The study concluded that SIRT6 activated microglia in the brain injury induced by LPS, and that the SIRT6 activator MDL-811 decreased neuroinflammation. Other cells could also be involved. Researchers have created microglial SIRT6 knockout mice to pinpoint the different types of cells involved. However, they did not completely exclude other signaling pathways.
Inflammation has been linked to stroke, which is the second leading cause of death around the world. Neuroinflammation that is overactive is slowed down by the SIRT6 activator MDL-811. Other studies have found that the inhibitor MDL-811 blocks the innate immune memory responses of monocytes after BCG vaccination or stimulation with ligands. This is the reason why SIRT6 could be a promising clinical target.
MDL-811 Activator for SIRRTP-SIRT6-HIV healing requires the creation of blood vessels. This process is important for healing wounds, and MDL-800 enhances angiogenesis as well as vascular network reconstruction. The 25 mg MDL-800 group was more dense and had more Neovascularization. These results indicate that MDL-800 is an effective treatment option for wounds.
In mice, MDL-811 helps to promote long-term functional recovery after stroke. MDL-811 reduces the volume of infarcts as well as improves the sensorimotor functioning and lowers body weight. It also inhibits NF-kB signaling. These results suggest that MDL-811 may be a viable therapeutic option for patients suffering from stroke or other inflammation-related disorders. These promising results merit further investigation.
Free fatty acids are important inhibitors of the SIRT6 gene. They reduce cell expansion in animal models through cutting down the growth of tumor-specific xenografts and suppressing FoxO3a's expression. MDL-811 may also be used to inhibit the growth of cancerous hepatocellular cells. Its liver effects include inhibition of FoxO3a and ERK1/2, as well as SIRT6-mediated acetylation of H3K9 through SIRT6.
SIRT6 is an indication that DNA repair can be initiated by the chromatin. When SIRT6 is present, it promotes base excision repair (BER) which is a type of repair that involves fixing DNA damage. However, as we age the effectiveness of BER decreases. Thus, SIRT6 could be overexpressed within senescent cells to increase the efficiency of BER.
SIRT6 is known to benefit DNA repair and is responsible for organizing proteins and attracting enzymes. SIRT6 plays a part in DNA repair in species that live longer. This gene could be an option for DNA repair interventions. The ability to repair DNA efficiently is crucial for the long-term viability. Because of this, organisms that have higher SIRT6 levels have evolved better regulators of DNA repair.
SIRT6 could be utilized in humans to increase our understanding of DNA repair. Although DNA repair has been proven to be possible, it is possible that our genes have evolved in order to adapt to our unique environment. The next step in our study is to examine how SIRT6 works with other species that live longer, such as the bowhead whale. The goal is to find an effective cure that can stop the numerous deaths caused by this disease.
SIRT6's ability to improve cell health is another advantage. The enzyme regulates the Nrf2 pathway. This pathway is responsible for SIRT6's antioxidant action. It also helps protect against aging. Mice deficient in SIRT6 exhibit metabolic disorders and other aging-related abnormalities. Male mice with high SIRT6 levels live longer.
It is well-documented that PQQQ's bioenergetic properties are well-established. Its bioenergetic benefits include its ability to be an anti-melanogenic agent, cell cycle regulator, the carrier of free radicals, an antioxidant and inducer of sleep. It also has numerous functional roles in the body including activating CREB and cAMP as well as reducing MDA and insulin resistance.
In this study, pyrroloquinoline quinine (PQQ) blocked UVA-induced aging of HDF cells. This compound was found to be associated with SIRT1/Nrf2/HO-1 signaling and SIRT6 signaling. These results suggest the possibility of a role for PQQ in older mice. However, further research is required to determine the effects of this compound on ageing and the progression of disease.
In a set of tests, PQQ inhibited proliferation of three cancer cell lines for 48 hours. The cells were analyzed in an ultra-microscopical field using the Cell-IQ test. Nine microscopic fields were used for each group. Panels A and A consist of A549 and Neuro-2A cells. Panel D illustrates the viability of three cancer cell lines and two normal cells. CCK-8 evaluated the viability of three cancer cell lines, as well as 2 normal cells.
This bioenergetic PQQ gene has the ability to be anchored to the transmembrane. The PQQ gene is a hydrophobic domain at the n-terminus. It also has an enzyme catalytic activity at the c-terminus. The C-terminal region of the gene is awash in active PQQQ residues. The PqqD protein is a 10-kDa-protein that is required for the production of PQQ. It is produced by the Leclercia species. QAU-66 cell , and it contains a 377 amino acid putative protein.
Sirt6 overexpression inhibited the process of aging of cardiomyocytes. However, the protein levels of Sirt6 were similar to those of the control group. So, the over-expression Sirt6 may block the aging process of cardiac tissue by blocking the pathological changes that are associated with senescence. It is crucial to consider the biomarker PQQ With SIRT6 in order to confirm the findings of this study.
The sirt1 and SIRT6 genes in human cells can be done using the corresponding RNA-based reagent kit. The mRNA extracted was then analyzed using flow cytometry. FlowJo software version 7.6.2 was used to analyze the results. These results might not be reproducible in other circumstances. These studies show the potential for PQQ With SIRT6 Marker to treat of cancerous cells.
PMID: 15795229 by Liszt G., et al. Mouse Sir2 homolog SIRT6 is a nuclear ADP-ribosyltransferase.
PMID: 16439206 by Mostoslavsky R., et al. Genomic instability and aging-like phenotype in the absence of mammalian SIRT6.
*More publications can be found for each product on its corresponding product page