Semaphorin-3A Antibodies

Semaphorin-3A (SEMA3A)

Involved in the development of the olfactory system and in neuronal control of puberty. Induces the collapse and paralysis of neuronal growth cones.

Could serve as a ligand that guides specific growth cones by a motility-inhibiting mechanism. Binds to the complex neuropilin-1/plexin-1.

Gene Information

Human
Gene Name:	SEMA3A
Uniprot:	Q14563
Entrez:	10371

Family

Belongs to:
semaphorin family

Alternative Names

(semaphorin) 3A; coll-1; collapsin 1; Hsema-I; Hsema-III; MGC133243; sema domain, immunoglobulin domain (Ig), short basic domain, secreted; Sema III; SEMA1; Sema3A; SEMAD; SEMAIII; SEMAL; Semaphorin 3A; semaphorin D; Semaphorin III; semaphorin L; semaphorin-3A; SemD

Molecular Weight

Mass (kDA):
88.889 kDA

Genomic Context

Human
Location:	7q21.11
Sequence:	7; NC_000007.14 (83955777..84515189, complement)

Subcellular Localizations

Secreted.

Diseases

• Nervousness
• Neoplasms
• Tissue Adhesions
• Malignant Neoplasms
• Tumor Angiogenesis
• Crest Syndrome
• Muscular Fasciculation
• Pathologic Neovascularization
• Neoplasm Metastasis
• Ischemia
• Cell Invasion
• Spinal Cord Injuries

• Pruritus
• Neoplasm Invasiveness
• Tumor Progression
• Mammary Neoplasms
• Cardiac Arrhythmia
• Dermatitis, Atopic
• Dermatitis

Pathways

• Axon Guidance
• Cell Migration
• Innervation
• Angiogenesis
• Regeneration
• Localization
• Pathogenesis
• Cell Adhesion
• Translation
• Transport
• Cell Death
• System Development
• Endocytosis

• Secretion
• Brain Development
• Cell Growth
• Rna Interference
• Nervous System Development
• Chemotaxis
• Cell Proliferation

PTMs

• Phosphorylation
• Cleavage

• Oxidation
• Myristoylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SEMA3A

Best Uses of the SEMA3A Marker From Boster Bio

In this article, we'll discuss Boster Bio's Anti-Semaphorin-3A (SEMA3A) Marker and its Applications in SLE, TLR-9 expression, and Memory B cells. The information presented is intended for scientists around the world. Read on to learn more. Also, be sure to check out our SEMA3A Marker FAQ.

Boster Bio's Anti-Semaphorin-3A SEMA3A Marker

The Anti-Semaphorin-3-A SEMA3A Marker from Boster Bio is a high-quality serum. It has been tested in ELISA and IHC assays. This serum is derived from a peptide that recognizes human SEMA3A. If a positive response is obtained, the anti-semaphorin antibody will recognize the peptide. To further confirm the reactivity of the antibody, you can purchase the blocking peptide, which is available at a reasonable price based on the length of the immunogen.

The Anti-Semaphorin-3-A (SEMA3A) Marker has been validated as an effective tool in the diagnosis and monitoring of SLE. It has shown significant correlations with disease severity and autoimmunity. It has been shown to bind to memory B cells, which means that it may be used as a therapeutic agent.

Semaphorins are membrane-bound proteins secreted by cells. They are involved in repulsive axon guidance during the nervous system's development. Semaphorins belong to two families of receptors, neuropilins and plexins. Plexin-A and Neuropilin-1 are two members of the Sema3 receptor complex. Neuropilin-1 binds directly to Sema3A, ensuring high-affinity binding. Neutralizing Sema3A causes profound increases in T cell proliferation.

The anti-Sema3A antibody is designed to detect sema3A and sSema4D in human blood. The antibodies were tested in mouse models of collagen-induced arthritis and were able to inhibit inflammatory responses in synovium. Sema4D levels were also correlated with markers of disease activity in patients with RA.

Applications in SLE

Several studies have demonstrated that the SEMA3A Marker is a regulatory molecule associated with disease severity and autoimmunity in SLE. It is expressed in the serum of patients with the disease and in healthy controls. It also negatively correlates with SLEDAI and is associated with decreased serum proteinuria and anticardiolipin antibodies. Moreover, it has been shown that patients with SLE have a decreased risk of developing thrombotic events.

Since SLE is a multifactorial disease, individual biomarkers are not sufficient for diagnosis and monitoring of disease progression. To improve therapeutic outcomes, a combination of relevant biomarkers is required. These biomarkers must be reliable, inexpensive, and easy to measure. In addition, they must be organ-specific to be of value for disease diagnosis and monitoring. Several challenges must be overcome before the SEMA3A Marker can be used to aid in this goal.

In the same study, the serum CXCL13 level was found to be a useful biomarker for the detection of active disease in SLE patients compared to healthy controls. The CXCL13 level was significantly higher in SLE patients and decreased in healthy controls. These studies demonstrated that the SEMA3A Marker may have a potential role in the diagnosis and treatment of SLE.

Using the SEMA3A Marker for diagnosis in SLE is a valuable step toward advancing diagnosis. This novel biomarker could provide a unique tool for identifying patients with the disease, and improve the quality of patient care. Researchers are currently working to standardize the SEMA3A Marker as a diagnostic biomarker in SLE. This may help in identifying SLE earlier, before the patient experiences symptoms.

TLR-9 expression

Sema3A is a key regulator of bone mass. Its level is closely correlated with the amount of bone cells and the sensory nerve system innervating the bone. Knockdown of Sema3A in mice led to reduced sensory innervation of the bone and diminished bone mass compared to wild-type mice. These findings suggest that Sema3A may influence bone integrity directly and indirectly.

The SEMA3A marker is a secreted soluble protein that initially was identified as an axonal guidance chemorepellent. However, its importance extends far beyond the nervous system, with various functions outside the nervous system. As a result, it plays a pivotal role in bone development and maintenance of adult normal bone mass. However, the best use of the SEMA3A marker lies outside the nervous system.

Increasing SEMA3A levels in bone tissue increases bone mass. Sema3A binding to the Nrp1 receptor on the membrane surface of osteoblasts and osteoclasts promotes osteoblast differentiation and inhibits the differentiation of osteoclasts. In addition, it activates the canonical Wnt/b-catenin signalling pathway. In addition, increased Sema3A expression results in enhanced osteoblast differentiation and normal sensory innervation of the bone.

Sema3A is a key player in the immune system and is an important factor for a variety of diseases. In this study, the SEMA3A marker was found in diaphysis of femurs and osteocytes. When USN and naringin were administered to rats, Sema3A protein expression significantly decreased in the USN group. The dose of naringin had a similar effect on Sema3A expression.

Memory B cells

A recent study has revealed that the SEMA3A marker is expressed in a subset of memory B cells, which have different expression patterns. The results suggest that these cells are distinct from naive B cells. The gene expression of the DN population includes the same genes as the DN1 subpopulation, but demonstrates a different pattern. The data also show that DN3 cells have a different expression pattern than DN1 or DN2, suggesting a distinct pathway of activation.

Memory B cells have two developmental branches, one associated with classical memory cells, and one associated with Age-related B cells. In addition, there are two clusters of DN cells. The DN4 population contains IgE-rich memory cells. This cluster appears to be the precursor of classical memory cells. Memory B cells and the SEMA3A marker were identified in the non-human primate model.

As mentioned earlier, sema3A is a good marker for SLE disease activity, and it has a regulatory mechanism. The protein decreases TLR9 expression in memory B cells from SLE patients. Moreover, the SEMA3A marker has shown therapeutic potential in SLE. However, further studies will focus on the exact mechanism of SEMA3A and the therapeutic potential in SLE.

SLE patients showed lower sema3A levels in their serum compared to healthy controls. These findings suggest that sema3A may have a role in SLE autoimmunity, and it may also play a role in self-tolerance. Additionally, sema3A protein expression in SLE patients may also be associated with reduced levels of MFI and NP-1 in SLE.

Renal damage

The SEMA3A marker induces massive transient proteinuria in kidneys, podocyte foot process effacement, and endothelial cell damage. The proteinuria and albumin/creatinine ratios were quantified four and twenty-four hours after injection. In the control kidney, SEMA3A-treated podocytes show normal foot processes, GBM, and endothelial fenestrations, as well as two linked foot processes.

The SEMA3A marker has been found in urine of diabetic rats, mice, and humans with advanced glomerulopathy. While no studies have shown a link between this protein and renal disease, the findings suggest that SEMA3A is a promising biomarker of acute kidney injury (AKI).

Earlier studies have found that SEMA3A delays proteinuria in mice. Injection of the cDNA of human sema3A delayed the development of proteinuria. Four mice developed proteinuria of +3 after injection of the SEMA3A marker at ten to twenty-two weeks of age, whereas non-treated mice had no proteinuria at these ages.

USEMA levels are positively associated with serum creatinine and urine albuminuria. Patients with both renal damage components had higher USemaCR levels. Interestingly, gender and presence of diabetes did not significantly affect USemaCR levels. Rather, the presence of an increased USemaCR was associated with an increased risk of both acute and chronic kidney damage. In addition, USEMA levels were significantly higher in patients with reduced eGFR and macroalbuminuria.

SEMA3A is a protein that regulates integrin function in endothelial cells. It also has been shown to be a potent vascular permeability factor. It is therefore not surprising that it affects the renal system. Although the SEMA3A marker has many useful properties, a further study is necessary to determine whether it is associated with renal damage. The SEMA3A protein has been implicated in various diseases.