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- Table of Contents
10 Q&As
Facts about Seizure 6-like protein.
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Human | |
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Gene Name: | SEZ6L |
Uniprot: | Q9BYH1 |
Entrez: | 23544 |
Belongs to: |
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SEZ6 family |
Acig1; AIG1; Aig1L; BSRP-B; seizure related 6 homolog (mouse)-like; seizure related gene 6-like; SEZ6L
Mass (kDA):
111.782 kDA
Human | |
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Location: | 22q12.1 |
Sequence: | 22; NC_000022.11 (26169462..26383597) |
Widely expressed, including adult and fetal brains and lungs. Not expressed in all lung cancer cell lines.
Endoplasmic reticulum membrane; Single-pass type I membrane protein.
The Seizure 6-like protein is detected by monoclonal or polyclonal antibodies. These antibodies can recognize the protein in many animal samples, and Boster Bio uses rabbit and mouse as model species for development of Seizure 6-like protein antibodies. Boster Bio also produces antisera against a number of animal proteins.
Antibodies against the Seizure 6-like protein (SEZ6L2) target a gene or protein in the body. The antibody can bind to Seizure 6L2-like protein in different animal samples and is monoclonal or polyclonal. Boster Bio develops SEZ6L2-abs using rabbits and mice as their test subjects. SEZ6L2 antibodies were used to determine the protein's identity and to measure its levels in serum.
SEZ6L and SEZ6L genes have been associated with bipolar disorder, epilepsy and febrile seizures. Three CUB domains are found in the extracellular regions of these proteins. These domains can be found in many cell surface receptors. Therefore, SEZ6/SEZ6L may act as a cell surface receptor. These antibodies target neuronal tissues. The antibodies detect BACE1 with high sensitivity.
BACE1 inhibition reduces the soluble BACE1-cleaved ectodomain of SEZ6 and SEZ6L. BACE1 inhibition also increases levels of SEZ6L and SEZ6L at neuronal surfaces. These results suggest that BACE1 inhibiting Seizure disease is an effective treatment. Although this research is preliminary, further studies are needed to determine whether the BACE1 inhibitor is effective in the treatment of the disease.
The antibodies that were created recognize endogenous SEZ6L, SEZ6L. These antibodies are specific and highly reactive. They can be used to diagnose and treat neurological disorders. These situations may be helped by the use of high-affinity primaries using the SEZ6L indicator. We describe the methods used for creating these antibodies. Continue reading for more information. Here are some benefits to using this marker.
For SEZ6L detection, the antibody detected two bands in WT and SEZ6 KO brains. The major band measured 160kDa, while 130kDa was the weakest. These bands were not detected in TKO brains, but remained unchanged in WT and SEZ6 KO brains. The major band, which was similar to SEZ6, was also highly N-glycosylated. EndoH couldn't remove glycosylation. However, the 130kDa spectrum was not consistent in experiments of deglycosylation and may be an immature.
High-affinity primaries antibodies also have the advantage that they are more precise. The antibodies have a higher affinity for the antigen than their antigen, making it more difficult to elute from the column. The antigen-specific primaries antibodies are then captured with greater sensitivity, and more reactivity. In contrast, low-affinity primary antibodies are less specific. The high-affinity primary antibodies using the SEZ6L marker are sensitive to a wide range of antigens, including a range of non-antibody-antigens.
A new method for determining the presence SEZ6L was developed. This method validated the roles of SEZ6L and SEZ6 as BACE1 substrates in vivo. Both antibodies were also reduced in BACE1-deficient mice's CSF. Therefore, they are useful tools for determining the level of BACE1 activity.
Availability of the SEZ6L marker in cancers is not yet known. The gene is essential for the development of the nervous system and LTP, and is linked to schizophrenia and Alzheimer's disease. Although it is not known what role SEZ6 plays in these diseases, it is known that its mutation is associated with poor prognosis for cancer. Scientists have only provided partial information about its function.
Although its functions in human brain are not understood, it is known to play a significant role in complement regulation. The SEZ6 transmembrane gene is a single span transmembrane proteins. It has an extended domain that includes five complement control domains and three CUBdomains. SEZ6 is also localized to the somatodendritic membrane of neurons.
The gene is involved in glycosylation of GluK2/3. SEZ6KO has two bands that affect GluK2/3. The enzyme EndoH converts the two bands into three distinct bands: the lowest band contains no mature sugar chains, while the two upper bands contain some mature sugar chains. SEZ6L, which is involved in the regulation glycosylation GluK2/3, is considered a key protein.
SEZ6 is necessary for the surface transport of GluK2 in neurons. SEZ6 promotes their trafficking by interacting with the trans-cisterna of the Golgi network. SEZ6 is also involved with the proper glycosylation GluK2 & GluK3 glucosides. The absence of SEZ6 in a cell can cause neurologic disorders.
The SEZ6L biomarker is a novel biomarker that has multiple applications. SEZ6L plays a role in motor coordination and inhibits anxiety-related behaviour. Movement disorders and neuropsychiatric illnesses may be caused by abnormal functions of the SEZ6L genes. SEZ6L has attracted attention in neurological research. It is a promising tool for neuropsychiatric disorders and movement disorders.
The SEZ6L gene, a transmembrane protein that spans a single span, has a large extracellular and three CUB domains and five Sushi domains. These domains represent typical features of proteins that are involved in protein-protein interaction. The SEZ6L gene may be expressed on neurons and act as a surface receptor. It is not known what SEZ6L does.
SEZ6L is expressed in high amounts in the cerebellum. This means that a deficiency results in significant changes to the cerebellum’s proteome and anatomy. We stained sections of wild-type and SEZ6L-knockout mice with calbindin and purkinje-cell-specific protein II, IP3 receptor, synaptophysin, and glial fibrillary acids protein to determine the level SEZ6L within cerebellar cortex.
SEZ6L plays a variety of functions, including motor control. Mice lacking all three members of the SEZ6 family display deficits in motor coordination on a rotarod and cognitive abilities. Single SEZ6LKO mice exhibit fewer severe phenotypes. This is likely because the SEZ6 family members perform redundant functions. A SEZ6 single-KO mouse line showed specific motor coordination defects, although further investigation is required.
PMID: 11175339 by Nishioka M., et al. Identification of a 428-kb homozygously deleted region disrupting the SEZ6L gene at 22q12.1 in a lung cancer cell line.
PMID: 12529303 by Collins J.E., et al. Reevaluating human gene annotation: a second-generation analysis of chromosome 22.