This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Facts about Anti-Muellerian hormone type-2 receptor.
Receptor for anti-Muellerian hormone. .
Human | |
---|---|
Gene Name: | AMHR2 |
Uniprot: | Q16671 |
Entrez: | 269 |
Belongs to: |
---|
protein kinase superfamily |
AMH type II receptor; AMHR2; AMHREC 2.7.11.30; AMHRII; C14; MIS RII; MISR2; MISRII; MISRIIMIS type II receptor; MRII; Muellerian hormone type II receptor; Muellerian hormone type-2 receptor; Mullerian hormone receptor, type II; Mullerian inhibiting substance type II receptor
Mass (kDA):
62.75 kDA
Human | |
---|---|
Location: | 12q13.13 |
Sequence: | 12; NC_000012.12 (53423855..53431672) |
Membrane; Single-pass type I membrane protein.
The AMHR2 Marker is the primary target of targeted vaccination against the hormone anti-Mullerian. This marker is used to develop vaccines as well as to conduct application-specific and species-specific research. In this article, we'll describe the most effective applications of the AMHR2 marker. This technology can be utilized by scientists all over the world. Read on to learn more. Also, find out how it compares with the ACVR2B marker.
The anti-Mullerian hormonal (AMH) is a protein produced by both the reproductive tissues of both the sexes. It blocks the growth and development of the Mullerian tubes in the male embryo. This can cause persistent Mullerian syndrome type II. AMH levels vary based on age and gender, and are crucial to the development of sex organs in the fetus's development. Anti-Mullerian hormone (AMH) levels are elevated in females who are affected by a mutation in the gene that encodes anti-Mullerian hormone.
Studies conducted in mice have shown that AMHR2-CD vaccination targeted to mice blocks tumor growth. AMHR2-CD vaccination decreased the overall burden of tumors and weight of the tumor. It also significantly prevented ID8 tumor growth. The development of a growing and visible EOCs from autochthonian EOCs was also stopped through vaccination. The mechanisms that underlie these effects remain under study. This study will continue to examine these questions.
A defined fragment of the ovarian differentiation protein, AMHR2-CD is expressed on around 20% of human EOCs. The AMHR2-CD vaccine offers prophylactic and therapeutic benefits in the treatment and prevention of cancer of the ovary. The vaccine caused minimal ovarian inflammation, which resolved quickly and did not impact fertility. The vaccine also triggered tumor growth but not enough to alter fertility.
In comparison to mice that were CFA-only-immunized and had significantly higher OS mice immunized with AMHR2-CD had significantly better OS. The results suggest that the treatment can protect against potentially fatal peripheral autoimmunity. AMHR2-CD vaccination does not cause nonovarian-associated autoimmune disease and the animals had similar litter numbers. Furthermore, AMHR2-CD-immunized animals had similar numbers of pups to CFA-immunized mice.
In addition to being highly effective targeted vaccination against AMHR2-CD can also be a safer alternative for treating patients suffering from EOC. If the condition is already known, this therapy may be sufficient to be administered to children. The AMHR2-CD targeted vaccination, a relatively new treatment for EOC is promising. Although research is still ongoing to determine the underlying mechanisms of AMHR2-CD vaccination, the possible benefits of targeted vaccination against this viral protein are clear.
To make a humanized variant of AMHR2-CD, the antigen has to first be recombinant. Humanization replaces the non-binding sequences in the mouse 4D12G1 Ab MAb with those of human. Thus, the antigen-antibody compound is absorbed into the cell and activated by caspase-3. The caspase-3 enzyme is activated, which cleaves PARP-1 and causes an apoptosis.
AMHR2-CD recognizes two AMH binding sites in the brain. One of these sites is KTLGELL26. It is located on the AMH CD molecule. The cell membrane contains four AMH-binding spots that are adjacent to each other. The weaker AMH-binding site is located near the AMH-ED receptor. AMH ligands can also be connected to both receptors.
Studies have shown that AMHR2-CD can be found in human skeletal muscle and the heart. A targeted vaccination against AMHR2 may be possible. Additionally various antibody-based treatments for SARS-CoV-2 are in clinical trials. These antibodies may be an interim solution. They won't eliminate SARS and CoV-2, but they can prevent future disease. These issues make it imperative to create a vaccine that targets AMHR2-CD's complex structure.
The ACVR2B/Fc protein, which was given to mice on the days L+35 and then L+42 was used to test comparisons with flight mice. The mice in the groups 4 and 5 received two injections of ACVR2B/Fc. These mice were kept alive at Explora under the same conditions as flight mice on board the ISS. Mice were imaged with the Piximus DXA scanner, and the weight of the muscles was assessed using the aid of a microCT. SomaScan was used to conduct RNAseq as well as ELISA.
ACVR2B/Fc treatment significantly decreased expression of the Cited4 and the Pfkm genes in skeletal muscles but it did not alter the phosphorylation. However, it did reduce the expression of mTORC1 as well as ERK. However, ACVR2B-Fc failed to significantly increase collagen deposition. This is crucial to further study. For the moment, ACVR2B is an intriguing alternative to other drugs.
The ACVR2B/Fc receptor for decoys is well-known to affect bone growth and homeostasis. In mice, ACVR2B/Fc treatment has significant effects on bone mineral density. As compared to mice living on Earth wild type mice treated with ACVR2B/Fc demonstrated significant decreases in bone mineral density. The results suggest that ACVR2B/Fc could be a powerful protection against bone loss that is caused by microgravity.
The Acvr2a subtype that binds to ligands mediates activin-A effects on myelination and differentiation of oligodendrocytes. In addition, blocking Acvr2a blocks actin disassembly in oligodendrocytes. Blocking Acvr2b decreases Acvr2b's expression and allows Acvr2a to be able more easily to bind to the ligand.
In mice, silencing ACVR2B led to a higher body mass and carcass characteristics than wild-type mice. While the total RBC count of both knockdown groups was not significantly different, they were both comparable in serum cholesterol as well as total WBC count. These differences were not statistically significant. Therefore, it is possible that the mice with ACVR2B silencing do not have the same gene. It is therefore unclear whether ACVR2B is needed to prevent the death of birds.
Inhibiting ACVR2A and MSTN genes resulted in significantly lower levels of protein and mRNA in the test group. The serum levels of ACVR2A and MSTN were higher in control birds than those of the knocked-down mice. The serum ACVR2B concentrations in knockdown mice were lower than those in control birds. Comparisons with knockdown mice also revealed that ACVR2B expression was associated with leg musclepercentage. The highest amount of protein is found in the ACVR2B gene.
PMID: 7493017 by Imbeaud S., et al. Insensitivity to anti-Muellerian hormone due to a mutation in the human anti-Muellerian hormone receptor.
PMID: 7488027 by Visser J.A., et al. Structure and chromosomal localization of the human anti-Muellerian hormone type II receptor gene.