Gremlin-1 Antibodies

Gremlin-1 (Grem1)

Cytokine that may play an important role during carcinogenesis and metanephric kidney organogenesis, as BMP a antagonist required for early limb outgrowth and patterning in keeping the FGF4-SHH feedback loop (PubMed:12808456, PubMed:15201225). Down-regulates the BMP4 signaling in a dose- dependent manner (PubMed:15133038).

Antagonist of BMP2; inhibits BMP2-mediated differentiation of osteoblasts (in vitro) (By similarity). Acts as inhibitor of monocyte chemotaxis (By similarity).

Gene Information

Mouse
Gene Name:	Grem1
Uniprot:	O70326
Entrez:	23892

Family

Belongs to:
DAN family

Alternative Names

Cell proliferation-inducing gene 2 protein; CKTSF1B1gremlin 1, cysteine knot superfamily, homolog; Cysteine knot superfamily 1, BMP antagonist 1gremlin 1, cysteine knot superfamily, homolog (Xenopus laevis); DAN domain family member 2; DAND2; DAND2GREMLIN; Down-regulated in Mos-transformed cells protein; DRM; DRMMGC126660; GREM1; gremlin 1; gremlin 1-like protein; Gremlin; gremlin-1; IHG-2; Increased in high glucose protein 2; increased in high glucose-2; proliferation-inducing gene 2

Molecular Weight

Mass (kDA):
20.71 kDA

Genomic Context

Mouse
Location:	2 E4|2 57.43 cM
Sequence:	2;

Tissue Specificity

Highly expressed in spleen and to a lesser extent in lung, skeletal muscle and kidney. Expressed only in non- transformed cells or primary fibroblasts in culture but not in established transformed or tumor derived cell lines. Broadly expressed in limb bud mesenchyme but restricted to the distal limb bud mesenchyme and concentrated posteriorly. Expressed in ovary especially in granulosa cells of follicles of type 4.

Diseases

• Malignant Neoplasms
• Kidney Diseases
• Neoplasms
• Diabetic Nephropathy
• Carcinoma
• Fibrosis
• Colorectal Cancer
• Cell Transformation, Neoplastic
• Carcinogenesis
• Tumor Angiogenesis
• Diabetes Mellitus
• Hypertrophy

• Colorectal Neoplasms
• Kidney Failure, Chronic
• Fracture
• Pulmonary Fibrosis
• Congenital Abnormality
• Hypertensive Disease
• Malignant Neoplasm Of Stomach

Pathways

• Limb Development
• Pathogenesis
• Angiogenesis
• Cell Proliferation
• Regeneration
• Kidney Development
• Secretion
• Embryo Development
• Fertilization
• Methylation
• Cell Cycle
• Localization
• Lung Development

• Cell Differentiation
• Tissue Homeostasis
• Transdifferentiation
• Bmp Signaling Pathway
• Tissue Remodeling
• Cell Growth
• Rna Interference

PTMs

• Phosphorylation
• Methylation

• Glycosylation
• Cleavage

Research Areas

• Neuroscience

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Grem1

Best Uses of the GREM1 Marker

This article will review the Molecular Mechanism of the GREM1 marker. It will also provide information on Immunohistochemical Assays, as well as cell targeting. To learn more, please visit Boster Bio. Best Uses of the GREM1 Marker

Molecular Mechanism

The promising therapeutic target for cancer treatment is the Molecular Mechanism of GREM1 marker. This gene binds to the EGFR which plays a major role in the initiation of cell growth and proliferative. In addition, GREM1 interacts ERRa, which is an upstream regulator of GREM1 activity. GREM1 is thus a potent ERRa target gene.

GREM1 is known to inhibit BMP2, BMP4 & BMP7 and plays an important role in the process of cell differentiation. Cancer cells from 66cl4 showed upregulation of several stem cell markers and metastatic 66cl4 tumor cells had significantly elevated levels of Bmp4.

GREM1 is an important factor in the development and progression of glioma. GREM1 treatment is a fantastic alternative to improve the odds of survival for patients with this disease. There are many questions to be answered. Here are a few examples:

Gremin-1, a secreted protein, has been demonstrated to be associated with reduced relapse-free survival among ER-negative breast cancer patients. This association is maintained even when BMP-related gene levels are elevated in the tumor. This suggests that the underlying molecular reason for the expression of GREM1 in breast cancer is the formation of a tumor-infiltrating microenvironment that stimulates the GREM1 gene.

Recent research has demonstrated that Gremlin-1 increases EMT within human RPE cells. Gremlin-1 is an endogenous antagonist of BMP signaling. It also induces epithelium-mesenchymal transition in fetal RPE cells. This process can be stopped in cancerous tumors or inducible through siRNA. The recombinant Gremlin-1 enhances EMT.

There is evidence that GREM1 may be involved in the epithelial-mesenchymal transition (EMT). Gremlin-1 inhibition enhances the invasion and migration of tumor cells. When it is knocked out, it results in a decrease in viability and an increase in cell death. Furthermore, it inhibits TGF-b1's activation of Smad signaling pathways. These findings suggest that GREM1 could be a promising target for treating proliferative vitreoretinopathy. Gremlin-1 could play a part in fibrosis since it is a component of vitreoretinopathy.

One study found that patients who have a common GREM1 variant have a high probability of developing colorectal cancer. This variant of the GREM1 gene has been found in at least 33% of patients suffering from colorectal carcinoma. Additionally, it was discovered that the gene was altered in a family suffering from atypical polyposis syndrome. In the end, it is now part of a variety of multigene panels.

Clinical Applications

The GREM1 gene is a marker for colorectal cancer risk. It has been used to determine colorectal polyps in patients with an ancestral history of Lynch syndrome. Recently it was used to identify an uncommon phenotype known as POLE in patients with early-onset cancer. The GREM1 gene is also linked to HMPPS which is a marker for MSS.

The GREM1 gene is involved in regulating the BMP signaling pathway, which includes the BMP2 and BMP4 receptors. GREM1 also affects the PVT1 lncRNA and is associated with WHO grades III-IV glioma as well as para-carcinoma. In addition, miR-128-3p has been elevated in para-carcinoma and glioma tissues, suggesting that it promotes the proliferation and metastatic potential of glioma cell lines.

One study reported that nine of ten patients with SCG5-GREM1 duplication-associated polyposis had a mixed hyperplastic/inflammatory polyp. The Donating Investigator reported homozygotes are viable, but the Y chromosome could not be fixed in a background of C57BL/6J. This research has many implications for clinical practice. It is possible to track the prognosis of patients suffering from GREM1 duplication.

The GREM1 gene plays a significant role in the development of the cortical part of the brain. It also plays a significant role in the formation of excitatory neuroprogenitors. Thus, knowing the biological basis of this gene can aid in the development of novel therapies for neurological and neurodevelopmental diseases. At present, it is considered an extremely valuable gene to monitor. However, clinical applications are only beginning. The study of this gene is ongoing so keep your eyes peeled for more information!

Immunohistochemical Assays

The GREM1 Marker is a CAF-derived protein that has potent pro-tumorigenic effects. It plays an important role in the invasion and dispersal of cancerous cells. Boster Bio GREM1Marker tests are a great way to determine the expression of this protein in various cancerous tissues. They are therefore particularly useful in identifying breast cancer.

Grem1 is one of the transcription factors that triggers tumorigenesis and boosts mammosphere formation. Grem1 expression is associated with mesenchymal markers found in tumor samples which support the notion that Grem1 expression at the invasion front is one of the major factors that contribute to the poor outcome of cancer. This could help explain the clinical connection between Grem1 and poor MFS.

To conduct the GREM1 Marker immunohistochemical experiments, US Biomax offers tissue microarrays of breast cancer as well as adjacent normal tissues. The GREM1 RNA in situ hybridization (ISH) was conducted using RNAscope GREM1 Probe and 2.5 HD Detection Kit. Images of the blots have been captured using a Pannramic 250 Flash III. The number of punctate dots that were intracellular brown in the cancerous tissue was used to determine whether GREM1 was present.

Another GREM1 Marker immunohistochemical test was used in a study involving 19TT cancer cells and GREM1 knockdown/overexpressing cells. GREM1 Marker immunohistochemical tests used antibodies against phospho–SMAD1/5/8, GRPR and lysinehydralase as well as phospho–SMAD1 as control.

Cellular Targeting

Cellular Targeting using the GREM1 markers is a promising way to identify cancerous cells and detect them with minimal adverse effects. GREM1 is a secreted protein that plays a key role in epithelial-mesenchymal transition (EMT). However, there are a number of potential pitfalls that should be considered prior to implementing this method. This article will explore the key features of this innovative new method.

The treatment may increase the amount of lipid droplets that intestinal fibroblasts produce. It increases fatty acid oxidation by activating the MAPK pathway. While the function of GREM1 in fibrosis remains fully understood, it does help in the development of fibroblasts. Apart from its ability to increase lipid droplets, it is also able to lower the expression of FAO-associated enzymes a variety of fibrotic diseases.

Two cell lines were used in the study that included a healthy mouse that was used as a control and a C57BL/6J model of intestinal fibrosis. Mice treated with the drug suffered from severe colitis. The mice treated with DSS had a smaller body weight and shorter lengths of their intestinal. Sections of the intestine were stained with H&E and anti-a–SMA-IHC. In the intestines of mice, the GREM1 protein was also observed.

Genetic factors may contribute to the development of colon cancer. There are many genes that are highly susceptible for cancer, yet only a tiny percentage of patients have one. Genetics remains a nebulous process that causes colorectal polyps. A 40-kb duplicate in the GREM1 gene regulatory region was recently discovered in an Ashkenazi family suffering from polyposis syndrome that is atypical. The gene has been added to a variety of panel of cancer genes.

The study revealed that patients with high levels of GREM1 mRNA expressed poorer survival in general than patients with low levels. Western blot analysis also showed high levels of gremlin1 in patients with metastatic polyps. This suggests that the cancer cells expressed high levels of the gremlin1 gene, whereas 67NR showed low levels. A high Bmp4 expression was not related to a lower RFS.