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We validate the specificity of these antibodies to CYP11B1 by testing them on tissues known to express CYP11B1 positively and negatively. Browse below to find the CYP11B1 antibody that suites your experiment. We have 3 of these antibodies and many publications and validation images.
If you cannot find antibodies that fit your needs, contact us for making custom antibodies. We have a full suite of custom antibody services covering from research to diagnostic and therapeutic applications.
Facts about Cytochrome P450 11B1, mitochondrial.
|cytochrome P450 family|
CPN1; CYPXIB1; cytochrome P450 11B1, mitochondrial; cytochrome p450 XIB1; cytochrome P450, family 11, subfamily B, polypeptide 1; cytochrome P450, subfamily XIB (steroid 11-beta-hydroxylase), polypeptide 1; Cytochrome P450C11; Cytochrome P-450c11; EC 1.14.15; EC 184.108.40.206; FHICYP11B; FLJ36771; P450C11DKFZp686B05283; S11BH; Steroid 11-beta-hydroxylase; steroid 11-beta-monooxygenase
|Sequence:||8; NC_000008.11 (142872357..142879825, complement)|
Mitochondrion inner membrane; Peripheral membrane protein.
CYP11B1 is a member of the cytochrome P450 superfamily, and it is involved in migration and the production of ROS. It has many applications. In addition, it is applicable to all scientists in the world. We will be discussing some of the most effective uses of CYP11B1 for research. Read on to find out more!
The CYP11B1 cytoglobulin B1 marker is a highly-specific immunoglobulin. Boster Bio offers primary antibodies with high affinity and excellent cross-reactivity for use in Western Blotting, Immunohistochemistry, and ELISA. The CYP11B1 gene marker is one of most used in biological research.
The CYP11B1 (aldosterone synthesise) gene is closely related to the CYP11B1 (aldosterone syntheticase), which codes the same protein. Both genes map directly to chromosome 8,q21 and encode members in the cytochrome P450 suprafamily. These proteins are monooxygenases that catalyze drug metabolism and synthesis of cholesterol and lipids. The CYP11B1 CYP11B1 protein can be found primarily on mitochondria's inner membrane. It has been shown to be a key player in neointimal structures in male mice.
Boster Bio Acai berry extract assay - Best Uses CYP11B1-related neurotoxicity is highly correlated with polymorphisms in this gene. It has been shown that polymorphisms within the CYP3A5 genetic code and the ABCB1A6986G gene have a significant association after hematopoietic stem-cell transplantation with calcineurin-related neurotoxicity.
CYP11B1 and CYP3A5 polymorphisms were examined for their association with adverse outcomes in pediatric renal transplantation. Multiple linear regression analysis was used with the generalized estimating equation. Allelic discrimination assays were used to analyze the data. Higher trough Tac concentrations were seen in recipients and donors due to polymorphisms in CYP3A5 polymorphisms.
CYP11B1 is a gene encoding a molecule involved in steroid biosynthesis. This enzyme is located in the mitochondrial inner cell. Its primary function, however, is to catalyze cholesterol into pregnenolone. In this way, the CYP11B1 gene plays a vital role in the steroid biosynthesis pathway. It is located on chromosome 15,q24.1 and contains 10 exons. CYP11A1 is also known to be a risk marker for PCOS. This genetic variant increases the likelihood of PCOS when environment and genetics interact.
Several helminths are known to increase CYP11B1 oxidation. Oxidative metabolism has been linked with drug resistance. Some helminth species have been found to oxidize antihelmintics like phenytoin, albendazole, and clomipramine, forming a product called ABZ sulfoxide. Some species undergo enhanced oxygenation.
The mutation in CYP11B1 has a mutation in exon 8 of the gene, which affects its expression. The R448H mutation occurs in the CYP11B1 CYP11B1 genome at a highly conserved residue. Eleven out of the twelve mutant alleles were affected by the mutation. Most patients had previously reported the disease. Paperna et al. found two carriers of mutations. (2005).
Molecular analysis of CYP11B1 gene revealed that the enzyme is highly heritable. Imrie et.al. Imrie et al. found that the gene is closely related to mineralocorticoid metabolic. Its heritability was 52%. The strongest genetic association between genotype and THAldo was at the rs6387 Polymorphism, located within intron 3 of CYP11B1. The study also revealed a significant genetic link between the G allele and the T allele.
Although the function and mechanism of CYP11B1 are not known, many researchers believe it is involved with hematopoiesis or migration. The local renin-angiotensin system (RAS) contains proteins and peptides involved in hematopoiesis, migration, and thrombopoiesis. Most RAS molecules in mammals are found in the hematopoetic bones marrow microenvironment. They play a central role for cell division and migration.
Multiple cases of 11b-OHD were reported. The patient, a Croatian-born patient, was a compound heterozygous person for p.R141Q. (CYP11B1) A second patient had c.1200+4A>G, a novel intron7 mutation. This is the very first case of 11bOHD in Croatia. The mutations at CYP11B1 have caused a phenotype which includes a combination a variety of features.
CYP11B1 genes mutations have also shown associations with disease. Many of these mutations, while highly heritable, have a significant effect on the geography and demographics. The most common mutation, the p.R448H has been identified in Brazilian Jews and Moroccan Jews. Similarly, p.R448H and g.4671_4672insC have been reported in Croatian families.
Hampf et al. (2010) reported a case involving steroid-11-beta hydroxylase deficiency (202010). It was caused due to unequal crossover of CYP11B1 & CYP11B2. They discovered that genetic recombination effectively deleted the normal CYP11B1 gene and created a chimeric fusion DNA containing both genes. In the mutant, CYP11B1 activity had been subordinated and controlled by CYP11B2. Potassium and angiotensin are the primary regulators of the expression of CYP11B2 genes.
ROS, which are reactive oxygen compounds, are molecules that have varying degrees of oxidant activities and that can modulate cellular processes as well as redox-dependent signalling. Numerous antioxidant pathways maintain redox balance, and when this balance is disturbed, ROS are produced. ROS can cause damage to proteins, lipids and nucleic acid, which can lead to cell death and other diseases. ROS can be linked to diseases like diabetes mellitus (CVD), and neurodegenerative disorders.
ROS are formed during steroidogenesis. High levels of steroids can cause P450 hydroxylase to decrease, leading to ROS production. Another potential source of ROS in rodents is the cholesterol carrier, HDL3.
ABCD1 mutations lead to abnormal accumulations VLCFAs throughout the plasma and in various tissues, such as the adrenal cortex. These tissues are affected by oxidative stresses according to histology. These cells have higher levels of MnSOD as well as lipid peroxidation, ROS production, and decreased levels of GSH compared with WT fibroblasts. Patients with triple-A disease have been shown to experience failures in nuclear import of DNA repair protein and DNA ligase 1.
This study also demonstrated a role for CYP11B2 in a novel way. In a mouse model with CKD, elevated phosphate levels induced osteogenic reprogramming VSMCs. In addition, pharmacological inhibition of the mineralocorticoid receptor (MCR) prevented the phosphorus-induced osteogenic transformation of HAoSMCs, and deficient CYP11B1 inhibited both processes. These findings suggest that vascular regulation plays a significant role in osteogenic programming and calcification.
As the field of cancer research develops, scientists are developing new methods to treat the disease. Checkpoint inhibitors, which have been proven to be effective in treating certain types and types of cancers such as head and neck, bladder, and triple negative breast cancer, are one example. These therapies need to be adapted to specific patient populations. Scientists must understand the causes of cancer to develop new drugs. Scientists must work together and in teams to discover new ways to treat the disease.
Cancer gene therapy involves modifying the T cells in a patient's body to attack cancer cells. Cancer cells that have faulty genes can cause tumors to grow out of control. Cancer gene therapy replaces the damaged genetic information with new, healthy code. While the process is still being developed, the basic principle of the process remains unchanged. Researchers use cancer gene therapy to add or delete genes, modify genomes or remove entire segments or parts of DNA. The new gene would be introduced into the cancer cells, which would cause the cells to die and prevent further growth of the disease.
Some researchers are also using specialized bacteria to help with cancer delivery. Prof. Simone SchurleFinke at ETH Zurich is one such researcher. She is one among many scientists working to develop new drugs for cancer using magnetically responsive bacteria. Although scientists have known since the ages that certain bacteria colonizes tumors, their current use is revolutionizing cancer treatment. The researchers are able to deliver a therapeutic effect thanks to the use of modern genetic engineering.