Protein Wnt-5a Antibodies

Protein Wnt-5a (WNT5A)

Can trigger or inhibit canonical Wnt signaling, depending on receptor context. In the presence of FZD4, activates beta-catenin signaling.

In the presence of ROR2, inhibits the canonical Wnt pathway by promoting beta-catenin degradation via a GSK3-independent pathway that involves down-regulation of beta-catenin-induced reporter gene expression (By similarity). Suppression of the canonical pathway allows chondrogenesis to happen and inhibits tumor formation.

Gene Information

Human
Gene Name:	WNT5A
Uniprot:	P41221
Entrez:	7474

Family

Belongs to:
Wnt family

Alternative Names

hWNT5A; protein Wnt-5a; wingless-type MMTV integration site family, member 5A; WNT-5A protein; Wnt5a; Wnt-5a

Molecular Weight

Mass (kDA):
42.339 kDA

Genomic Context

Human
Location:	3p14.3
Sequence:	3; NC_000003.12 (55465715..55505261, complement)

Tissue Specificity

Expression is increased in differentiated thyroid carcinomas compared to normal thyroid tissue and anaplastic thyroid tumors where expression is low or undetectable. Expression is found in thyrocytes but not in stromal cells (at protein level) (PubMed:15735754). Detected in neonate heart and lung (PubMed:8288227).

Subcellular Localizations

Secreted, extracellular space, extracellular matrix. Secreted.

Diseases

• Malignant Neoplasms
• Neoplasms
• Neoplasm Metastasis
• Carcinoma
• Cell Transformation, Neoplastic
• Malignant Paraganglionic Neoplasm
• Tissue Adhesions
• Cell Invasion
• Melanoma
• Malignant Neoplasm Of Breast
• Mammary Neoplasms
• Neoplasm Invasiveness
• Carcinogenesis

• Skin Neoplasms
• Leukemia
• Inflammation
• Malignant Neoplasm Of Stomach
• Malignant Tumor Of Colon
• Malignant Squamous Cell Neoplasm
• Adenocarcinoma

Interacting Proteins

• WIF1

Pathways

• Cell Proliferation
• Cell Migration
• Localization
• Cell Growth
• Secretion
• Cell Adhesion
• Pathogenesis
• Gastrulation
• Convergent Extension
• Cell Differentiation
• Methylation
• Cell Cycle
• Cell Motility

• Regeneration
• Osteoblast Differentiation
• Angiogenesis
• Neurogenesis
• Endocytosis
• Axon Guidance
• Wound Healing

PTMs

• Phosphorylation
• Methylation
• Cleavage
• Demethylation
• Glycosylation

• Acetylation
• Palmitoylation
• Formylation
• Ubiquitination
• Biotinylation

• Reduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/WNT5A

Best Uses Of The WNT5A Marker

WNT5A is a key signaling molecule that regulates neuronal outgrowth and neuronal polarization, is important. It activates the non-cannonical Wnt/calcium pathway within cells. It also blocks the apoptotic reaction of fibroblasts and activates Wnt5a/PKC. However, the precise roles of WNT5A are not clear, but scientists have identified certain biological functions as well as its applications.

ELISA method

The WNT5A marker is a cell cycle regulator which is responsible for the progression of tumors and metastasis. The molecule triggers the release of pro-angiogenic as well as immunomodulatory factors from the exosomes of tumor cells. Inhibitors of cAMP-dependent kinase (IKK) block the WNT5A-induced release from exosomes.

The WNT5A-Rac1-Disheveled signaling circuit regulates autophagy in host macrophages. This circuit can limit infections caused by bacteria by preventing the growth of pathogens caused by bacteria. The role of WNT5A in autophagy is well known, but there is a lack of information about its function in autophagy. It will be important to investigate how WNT5A signals are used in autophagy , in the coming studies.

The ELISA test for WNT5a is an enzyme-linked immunosorbent technique that can detect WNT5A in human blood. Human cells are a model for the growth of tumor cells. An ELISA kit that detects the WNT5A marker in human fibroblasts will detect it. The ELISA can be used in conjunction with a suitable sample to provide an exact and consistent test result.

A 96-well ELISA was used to detect the WNT5A protein. The sample was coated onto the plate with 96 wells and followed by a probe using the appropriate antibodies. After six hours the samples could be washed with 0.1% Tween-20 in PBS. Then, they were processed with the help of a fluorescence microscope, an Olympus Fluoview FV10i equipped with a 60x objective as well as 3.4x Zoom. Each cell was counted for one time and the results were then compared across five fields.

Excellent technique is the ELISA method of detecting WNT5a in human HUVEC cells. It can also be used to identify cells that express Wnt5a and Wnt-1. WNT proteins can be found in more than 100 cell types that are not Wnt5a. The cells express higher levels WNT proteins compared to cells that are in the control infection.

Multiple scientists have validated the ELISA method for detecting WNT5a. This study demonstrates that WNT5A is linked to endothelial cell selective adhesion molecule expression in two types malignant melanomas. It is also linked with sepsis, COPD, and a variety of pathogenic bacteria.

WNT5A signaling can promote tumor metastasis. It may also trigger local and systemic immune suppression that allows tumor cells to evade immune recognition. The increased expression of WNT5A is associated with a lower prognosis in patients with melanoma. Further, it has also been proven that patients with high levels of WNT5A expression have worse prognosis. Malignant melanomas are known to be a carrier of the WNT5A gene, which is linked to metastasis.

The WNT5A gene is responsible for the regulation of endothelial cell growth, migration, as well as survival. It also regulates genes involved in angiogenic development. Moreover, reduced Wnt5a expression inhibits vascular regeneration. A study on this gene has revealed that WNT5a is activated by noncanonical Wnt signaling to encourage angiogenesis. This study also provided new insights into the control of the growth of endothelial cells.

Targeting Wnt5a/PKC signaling

Inhibitors of WNT5a/PKC signaling have been demonstrated to reduce Snail expression in melanoma cells. However, inhibitors of WNT5a/PKC signals alone weren't enough to stop the growth of melanoma cell lines. Melanoma cells can be stopped from migrating and metastasizing by inhibiting WNT5a/PKC signals.

To examine the role played by PKC signaling in lung cancer stem cells, researchers employed an assay for cell culture that measures colony-forming capacity. Researchers used a cell culture test to determine whether inhibitors of the WNT5a/PKC signaling pathway boosted A549 cell colony formation, while PKC inhibition slowed the migration and invasion of A549/DDP cells. In addition, targeting the WNT5a/PKC signaling prevented the development of chemoresistance in lung cancer cells.

The inhibitors blocked WNT3A activity but had no impact on WNT5A activity. The molecule inhibited WNT3A activity by five times. WNT5a/PKC-signaling inhibitors raised total PKC levels, while decreasing levels of phosphorylated proteins. This indicates that WNT5a/PKC inhibitors are extremely specific for WNT5a-targeted cancer cells.

WNT5A inhibits ROR1- and WNT5adependent genes. It also blocks genes that are regulated by WNT5A which include CD44 and vimentin. These inhibitors block WNT5A when WNT5A is blocked. Targeting WNT5a/PKC signaling in Boster Bio is an intriguing option for treatment of cancer.

Inhibition of PKC blocks MMP-2 production as well as the morphology of WNT5Ahigh cells. It can be used to kill cancerous cells by triggering WNT5A-targeted growth. Inhibitors of Wnt5a receptors that are targeted by PKC also block the function of MITF which is a crucial signaling molecule that causes cell mobility and invasion.

The gene Wnt5a regulates the expression of various proteins, including E.cadherin and CD44. It is implicated in the epithelial-mesenchymal transition, which is the precursor to metastasis. Several changes in protein expression are associated with EMT which includes the loss of E-cadherin. Transfected cells showed Wnt5A/A2 siRNA reductions in Wnt5A protein levels by 24 hours, 48 h and 48 h.

Pharmacological JNK antagonistic antagonism in mice inhibited the function of the vascular endothelial cells. In addition the an pharmacological JNK antagonists blocked insulin-mediated pNOS activation, which could be an avenue for treatment for the vascular diseases associated with obesity. However, further studies are needed to determine whether this inhibitor is effective in human studies.

In addition to reducing the cytotoxicity of MAPK inhibitors, MITF also contributes to paracrine defense by reducing ERK and BRAF signalling. Targeting EDNR and WNT5a/PKC signalling within Boster Bio is an ideal strategy to improve the efficacy of BRAF inhibitors. What are you waiting for Do you want to delay the effects of BRAF inhibitors? Get started today!

Clinical applications

The WNT5A marker is a molecular marker that is expressed in the early stages of bone growth. It is expressed mostly by osteoblastic niche cells bone marrow cells. It has been proven that it may preserve the stem cells of bone marrow and trigger osteoblast maturation. The protein also plays an important role in osteoblastogenesis mediated by bone morphogenetic protein 2.

The Wnt5A gene could be a target for therapeutic intervention in inflammation-related diseases. This marker is produced in substantial amounts by macrophages and synoviocytes in patients suffering from septic. The interference with this signaling pathway is thought to act in the very beginning of macrophage activation. This pathway isn't redundant, but the Wnt5A gene is thought to play important roles in the prevention of infection.

Through interaction with FZD5 and LRP5 In conjunction with the LRP5 or FZD5 proteins, the WNT5A protein interacts with LRP5 or FZD5 to bind eMSCs to itself. Scientists might be able to understand the role of this protein for stem cell regulation through the use of siFZD5 in order to produce the eMSC. WNT5A interacts with WNT5A to make the WNT5A gene expression feasible in eMSC. Additionally, WNT5A is known to regulate the activity of eMSC.

Numerous important roles play the WNT5A gene in the field of cancer biology. It has been discovered to be involved in chemoresistance, and is associated with a myriad of cancers. But, it's also involved in the suppression of rheumatoid arthritis, epithelial ovarian cancer. Clinical applications of WNT5A are rapidly growing.

Recently, Wnt5a was discovered to increase the activity of CYP and reduce the sensitivity of ER-positive breast cancer cells to drugs. Despite these findings, there have been fewer studies. Breast cancers with PI3K-AKT-mTOR-inactivated mutations and Wnt5a upregulation exhibit poorer prognosis. The same is true for ER-positive, pancreatic cancer.

Inhibiting TGFb1 signaling is one approach to target Wnt5a. The Wnt5a-related phenotype of melanoma cells may be able to be targeted with a new drug. Wnt5a plays an important role in metastatic development of cancer cells, and a drug targeting this gene could prove effective. It has been demonstrated that Wnt5a is a key factor in cell migration in various types of cancer.