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- Table of Contents
Facts about Medium-chain specific acyl-CoA dehydrogenase, mitochondrial.
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Human | |
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Gene Name: | ACADM |
Uniprot: | P11310 |
Entrez: | 34 |
Belongs to: |
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acyl-CoA dehydrogenase family |
ACAD1; acyl-CoA dehydrogenase, C-4 to C-12 straight chain; acyl-Coenzyme A dehydrogenase, C-4 to C-12 straight chain; EC 1.3.99; EC 1.3.99.3; FLJ18227; FLJ99884; MCADFLJ93013; MCADH; medium-chain specific acyl-CoA dehydrogenase, mitochondrial
Mass (kDA):
46.588 kDA
Human | |
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Location: | 1p31.1 |
Sequence: | 1; NC_000001.11 (75724347..75763679) |
Mitochondrion matrix.
This article provides information on ACADM Marker, Steven Boster and SO-RB50 cell assay. It also discusses Acad10 antibody and other important aspects of the cell assay. It covers the ACADM Marker's application and scientific value. You'll also learn how it can be used for scientific research. This information is relevant to scientists worldwide. We'll explore the details of ACADM Marker, SO-RB50 cell assay, and its various uses.
The IHB's annual markers installation program has increased dramatically over the last several years. While submitting a Marker Application is the first step, it is by no means a guarantee of approval. The IHB carefully reviews each application and the number of applications approved to move forward in 2022 will depend on the quality of the submitted applications. The applicant is required to provide reliable primary source materials and provide evidence of the importance of the proposed marker's location and function. The IHB staff will also perform the final research to ensure the marker is an appropriate fit.
The ACADM marker can be used to distinguish between memory B cells and other types of B cells. The memory B cells were observed to have a short-lived IgM+ and stable IgA+ memory, respectively. Furthermore, the memory B cells were specific to RBD or nucleocapsid. Moreover, the ACADM marker is able to detect cellular changes that are caused by a variety of diseases, including HIV.
SO-RB50 cells were transfected with pcDNA3.1-Rb1 and fixed with 75% ice-cold ethanol in PBS. The cells were then washed twice with PBS and stained with propidium iodide in a solution that contains EDTA and Triton X-100. The cellular morphology of the cells was determined by counting the number of colonies.
Inhibition of SUZ12 inhibited SO-RB50 cell invasion, and it suppressed the expression of MMP-9, MMP-2, and VEGF. These markers are associated with RB invasion and are expected to be involved in targeted therapy. However, the SUZ12 gene is not essential for the RB cell invasion and migration. Therefore, SUZ12 knockdown is needed to validate the Boster Bio SO-RB50 cell assay.
The SO-RB50 cell assay shows that the presence of exogenous Rb1 does not affect non-homologous end joining, but promotes homologous recombination. Using ACADM as a marker, we found that SO-Rb50 cells transfected with pcDNA3.1-Rb1 do not show significantly higher levels of HR compared to the controls. The results of this study are in line with previous studies showing that exogenous Rb1 does not affect direct DNA repair.
SUZ12 has been previously implicated in cancer development and phenotype, but has not been studied in retinoblastoma. It regulates matrix metalloproteinase and vascular endohydrohydroproteinase. Moreover, suppression of SUZ12 inhibits MMP-9 and VEGF expression. Therefore, it is important to analyze the effects of SUZ12 knockdown in a cell assay before determining which drugs are effective for cancer treatment.
Exogenous Rb1 suppresses growth of SO-RB50 retinoblastoma cells by inhibiting the expression of the Rb1 protein. The mutation was confirmed by immunofluorescence staining. The cells expressing the Rb1 protein are insensitive to ACADM. The cells are thus inactive in this case, but this is not indicative of cancer treatment.
PMID: 3035565 by Kelly D.P., et al. Nucleotide sequence of medium-chain acyl-CoA dehydrogenase mRNA and its expression in enzyme-deficient human tissue.
PMID: 1731887 by Zhang Z.F., et al. Structural organization and regulatory regions of the human medium- chain acyl-CoA dehydrogenase gene.