GDF15 Antibodies

Growth/differentiation factor 15 (GDF15)

Regulates food intake, energy expenditure and body weight in response to metabolic and toxin-induced stresses (PubMed:28953886, PubMed:28846097, PubMed:28846098, PubMed:28846099, PubMed:23468844, PubMed:29046435). Binds to its receptor, GFRAL, also activates GFRAL-expressing neurons localized in the area postrema and nucleus tractus solitarius of the brainstem (PubMed:28953886, PubMed:28846097, PubMed:28846098, PubMed:28846099).

It then triggers the activation of neurons localized inside the parabrachial nucleus and central amygdala, which contitutes part of the'emergency circuit' that shapes feeding responses to stressful conditions (PubMed:28953886). On hepatocytes, inhibits growth hormone signaling (By similarity).

Gene Information

Human
Gene Name:	GDF15
Uniprot:	Q99988
Entrez:	9518

Family

Belongs to:
TGF-beta family

Alternative Names

GDF15; GDF-15; growth differentiation factor 15; growth/differentiation factor 15; Macrophage inhibitory cytokine 1; MIC-1; MIC-1NSAID-activated gene 1 protein; MIC1Prostate differentiation factor; NAG-1; NAG-1NSAID-regulated gene 1 protein; NSAID (nonsteroidal inflammatory drug)-activated protein 1; PDF; PDFGDF-15; PLAB; PLABNRG-1; Placental bone morphogenetic protein; Placental TGF-beta; PTGF-beta; PTGFBPTGF-beta

Molecular Weight

Mass (kDA):
34.14 kDA

Genomic Context

Human
Location:	19p13.11
Sequence:	19; NC_000019.10 (18382170..18389176)

Tissue Specificity

Highly expressed in placenta, with lower levels in prostate and colon and some expression in kidney (PubMed:9348093). Detected in plasma (at protein level) (PubMed:28572090, PubMed:29046435).

Subcellular Localizations

Secreted.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Malignant Neoplasm Of Prostate
• Prostatic Neoplasms
• Inflammation
• Cell Transformation, Neoplastic
• Colorectal Cancer
• Malignant Tumor Of Colon
• Colorectal Neoplasms
• Neoplasm Metastasis
• Malignant Neoplasm Of Breast

• Malignant Paraganglionic Neoplasm
• Anemia
• Mammary Neoplasms
• Heart Failure
• Adenocarcinoma
• Carcinogenesis
• Hypoxia

Interacting Proteins

• MDFI

Pathways

• Cell Proliferation
• Cell Cycle
• Cell Growth
• Secretion
• Cell Death
• Cell Cycle Arrest
• Induction Of Apoptosis
• Pathogenesis
• Methylation
• Angiogenesis
• Macrophage Activation
• Wound Healing
• Localization

• Gene Silencing
• Senescence
• Rna Interference
• Cell Migration
• Regeneration
• Dna Methylation
• Dna Repair

PTMs

• Phosphorylation
• Cleavage
• Methylation
• Demethylation
• Reduction

• Glycosylation
• Deacetylation
• Acetylation
• Oxidation
• Dephosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/GDF15

Best Uses Of The GDF15 Marker

This article will discuss the many uses of GDF15 mark. This protein inhibits chemokine signaling by blocking activation of b2-integrin/lymphocyte function-associated antigen 1 (LFA-1) and the recruitment of infiltrating pro-inflammatory cells. Learn about the role played by GDF-15 in immunotherapy for cancer, and the limitations of its entry into organs that are infiltrating.

GDF-15 blocks chemokine signals

Boster Bio GDF-15 is a potent chemokine inhibitor that can also limit leukocyte recruitment. It does this by preventing chemokine signaling and limiting the activation of the LFA-1 receptor, which regulates the recruitment of the inflammatory cells. These findings provide a unique method to explain GDF-15's anti-inflammatory properties.

GDF15's function is not clear However, it is involved in a variety of biological processes. Certain studies have demonstrated that GDF15 inhibits chemokine signaling in mitochondrial disorders, which are known to be a problem for organs with high energy demands. These studies, while complex suggest that GDF-15 might play a role in many age-related diseases. It has been proven that GDF15 inhibits chemokine signaling, and it has also been demonstrated to inhibit activation of T cells.

GDF-15 has been proven to block chemokine production in mice and inflammatory processes in rats. Although its role is largely unknown, it has been implicated in the immunotolerance. In pregnant women, GDF-15 serum levels are elevated at the beginning of pregnancy and peak around the third trimester. Additionally women who had miscarried later had lower levels of GDF-15 in their blood.

The enzyme angiotensin receptors synthesize the protein and regulate vascular contractions and relaxation. It increases NO release. In mice, mice with GDF-15 knockout did not exhibit hemodynamic effects when tested in a genetic model. While GDF15 is not expressed in control animals however, it is released after injury and can increase NO levels. These effects are linked to the role of GDF15 and ErbB receptors in cell proliferation.

It inhibits b2-integrin/lymphocyte function-associated antigen 1 (LFA-1) activation

Lymphocytes play a variety of functions in the body and are responsible for controlling the flow of immune cells. Cell membranes contain receptors, referred to as integrins. In the state of rest they are in a bent, inactive shape. The receptors are activated in similar fashion to a switchblade, and they are in a favorable position towards the ligand on opposing cell.

BBI induced macrophages to express APOBEC3F, APOBEC3G. BBI also increased the phosphorylation of IRF3, which is a key regulator of IFN-I2 secretion. The effect was negated when compared with neutralization antibodies that inhibit the BBI-mediated induction of the anti-HIV factor. The findings suggest that BBI blocks several steps in the HIV replication cycle.

In addition to a study published in Nature The Boster Bio GDF15 inhibitors are now in the clinical trials of patients with a variety of immune system disorders. This treatment is based on the discovery of GDF15 inhibitors that inhibit b2-integrin/lymphocyte function-associated antigen 1 (LFA-1) activation.

In addition to regulating inflammatory processes, GDF-15 also regulates signaling pathways that are crucial to cardioprotection. It activates Smad and ALK type 1 receptors and forms a heteromeric complex that is associated with Smad 4. It also inhibits EGFR transactivation as well as the NF-B/JNK/caspase-3 pathway.

It reduces the recruitment of pro-inflammatory cells that infiltrate the infiltrating tissue.

There are numerous benefits of neutrophils in the body for instance, their ability to block the recruitment of pro-inflammatory cells. The acute inflammation response to infection plays crucial for neutrophils. Therefore, their elimination can increase the chance of infection and slow healing. These cells are useful in the treatment of inflammatory conditions such as EAE by regulating local immune reactions.

It also assists in the recruitment of monocytes as well as tissue-resident macrophages to sites of inflammation. Neutrophils also release mediators to aid in tissue healing, such as resolvins or protectins. Chronic inflammation is caused by neutrophils continuously migrating to inflammatory sites. They release serine proteases and traps that are extracellular which are involved in the process.

Neutrophils are the reason for adaptive immunity and the recruitment of monocytes in rheumatoid arthritis. However neutrophils also attract synovial fibrocytes, a form of cell that promotes adaptive immunity. Furthermore, neutrophils recruit monocytes, which possess an anti-inflammatory effect. Additionally, adaptive immunity is an defining trait of RA.

It inhibits EGFR transactivation

Boster Bio's GDF15 marker is a novel peptide that blocks EGFR activation. It has a broad functional scope. It regulates inflammation of the adipose tissue, prevents the proliferation of T cells, and ameliorates the metabolic syndrome. It is also a predictive marker of future type 2 diabetes and its severity. In actual fact it can delay the beginning of the disease in patients at risk.

GDF15 was discovered by several labs in the late 1990s. It was first discovered in the late 1990s as a regulator for macrophage activation, as well as a mediator between embryonic development and the placental life. It was later discovered to play an important role in various forms of cancer. Large-scale biomarker delineation showed that GDF15 expression was elevated in cancerous cells. Particularly the GDF15 expression was constant in pancreatic ductal adenocarcinoma, as well as prostate cancer.

In cervical cancer, GDF15 was associated with increased PI3K/AKT and MAPK/ERK activities. Furthermore, GDF15 inhibited EGFR transactivation by binding to the p-ErbB2 receptor. In breast cancer cells, GDF15 inhibited EGFR transactivation. This means that GDF15 might also inhibit tumor growth and spread.

It is a possible target for cancer immunotherapy

A new conference has been announced that will concentrate on GDF-15's potential as a therapeutic target for the treatment of cancer. The conference aims to explore the role of GDF-15 as a biomarker for PD1 inhibitors and also to present preliminary evidence indicating that GDF-15 could be a possible target for cancer immunotherapy. The conference will take place in Washington, D.C., between November 10 and 14, 2021. It can also be accessed online.

Previous studies have revealed that GDF15 is a key inhibitor of lung adenocarcinoma cells, and that it is an important regulator of the process of apoptosis. This increased activity of GDF15 is believed to be due to its protumoral role in human cancers. GDF15's bioactivity is linked to the TGF-b/Smad signaling pathway.

In addition to blocking cancer-causing ERK1/2, GDF15 is also known to enhance the formation of tumor spheres. The activation of GDF15 by ERK1/2 stimulates transcription of the protein. GDF15 circuits are necessary for cancer stem cells to grow and survive. Conventional chemotherapy is not capable of eliminating them. Cancer immunotherapy could be able of targeting GDF15 circuits and remove tumors. This is possible through neutralizing anti-GDF15 antibodies.

In the initial phase of the study, researchers determined that GDF15 regulates the expression of the p21 gene in cervical cancer cells. They also discovered that p21 expression is downregulated, and that GDF15 knockouts diminished the growth of tumors and metastatic potential. This suggests that YAP could promote the function of GDF15 by preventing transcription of a key gene, GDF15.

It may be used in monotherapy

Despite its limited use, Zonisamide could be a successful treatment option for different skin cancers. Studies have proven that the drug can improve the appearance and the quality of skin in some patients. The drug is also effective as an individual treatment, which can be beneficial in certain situations. Patients who could not take multiple drugs were included in the study. It can be used in conjunction with other drugs to offer more effective treatment.