ROR1 Antibodies

Inactive tyrosine-protein kinase transmembrane receptor ROR1 (ROR1)

Has very low kinase activity in vitro and is unlikely to be a tyrosine kinase in vivo (PubMed:25029443). Receptor for ligand WNT5A which trigger downstream NFkB signaling pathway and might result in the inhibition of WNT3A-mediated signaling (PubMed:25029443, PubMed:27162350).

In inner ear, crucial for spiral ganglion neurons to innervate auditory hair cells (PubMed:27162350). .

Gene Information

Human
Gene Name:	ROR1
Uniprot:	Q01973
Entrez:	4919

Family

Belongs to:
protein kinase superfamily

Alternative Names

EC 2.7.10.1; MGC99659; neurotrophic tyrosine kinase receptor-related 1; Neurotrophic tyrosine kinase, receptor-related 1; NTRKR1; NTRKR1dJ537F10.1; receptor tyrosine kinase-like orphan receptor 1; ROR1; tyrosine-protein kinase transmembrane receptor ROR1

Molecular Weight

Mass (kDA):
104.283 kDA

Genomic Context

Human
Location:	1p31.3
Sequence:	1; NC_000001.11 (63774017..64181498)

Tissue Specificity

Expressed strongly in human heart, lung and kidney, but weakly in the CNS. Isoform Short is strongly expressed in fetal and adult CNS and in a variety of human cancers, including those originating from CNS or PNS neuroectoderm.

Subcellular Localizations

Membrane; Single-pass type I membrane protein. Cell projection, axon.

Diseases

• Malignant Neoplasms
• Leukemia
• Lymphoid Leukemia
• Chronic Lymphocytic Leukemia
• Neoplasms
• Nervousness
• Acute Lymphocytic Leukemia
• Lymphoma
• Malignant Neoplasm Of Stomach
• Cell Invasion
• Malignant Neoplasm Of Breast
• Plant Diseases
• Malignant Paraganglionic Neoplasm

• Malignant Lymphoma, Lymphocytic, Intermediate Differentiation, Diffuse
• Chromosomal Translocation
• Malignant Neoplasm Of Lung
• Tissue Adhesions
• Crest Syndrome
• Stomach Neoplasms
• Neoplasm Metastasis

Interacting Proteins

• EGFR
• SRC
• Src

Pathways

• Localization
• Gene Silencing
• Methylation
• Cell Migration
• Dna Methylation
• Glycosylation
• Cell Death
• Secretion
• Cell Adhesion
• Cell Division
• Convergent Extension
• Dna Repair
• Complement-dependent Cytotoxicity

• Dna Replication
• Brain Development
• Antibody-dependent Cellular Cytotoxicity
• Cell Growth
• Rna Interference
• Transposition
• Neural Tube Closure

PTMs

• Phosphorylation
• Methylation
• Glycosylation
• Acetylation

• Biotinylation
• Cleavage
• Deacetylation
• Ubiquitination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ROR1

Best Uses of the ROR1 Marker

The ROR1 marker is an inactive tyrosine-protein kinase transmembrane receptor, and there are several biological tests that use it. Boster Bio creates antibodies against this protein by using mouse and rabbit samples. Although ROR1 is not a tyrosine kinase in the living environment, it is crucial for the innervation of auditory hair cells, just as is the case with other receptors.

ROR1 is an inactive protein tyrosine transmembrane kinase receptor

The inactive tyrosine-protein-kinase transmembrane (Tm) receptor ROR1 is a member of the tyrosine-protein kinese family, a large subfamily of tyrosine-protein kine receptors. Although the Tm members of the family are closely connected, ROR1 is unique in that it has no detectable catalytic activity. The expression of ROR1 in human cancer cells has been linked with high-grade tumors as well as poor clinical outcomes. ROR1 is a major component of cancerous cells, including cancer cells and has been implicated in the pathophysiology of chronic lymphocytic Leukemia (CLL).

Despite its low level of expression, wild-type ROR1 was located at the plasma membrane, whereas its mutant form showed decreased expression at the plasma membrane. The mutant ROR1 increased ubiquitination probably due to substrate protection or misfolding. However, ROR1 didn't activate the transcription factor NFKB in the presence of WNT5A which is a well-known ligand for WNT-interacting TPKs.

ROR1 is a potential target to target the Wnt pathway that promotes tumors. While the Wnt signalling pathway is recognized as being associated with many Gynecological tumors, ROR1 as well as ROR2 receptors are both potential therapeutic targets. The knockdown of ROR1 or ROR2 decreases the proliferation of KLE cells and also reduces the glioblastoma cell's migration and invasion. Further studies of ROR1 and ROR2 knockdowns may allow for greater understanding of function of ROR1 and ROR2 receptors in these tumors.

Although the biology and expression patterns of ROR1 are not fully understood Recent research suggests that monoclonal antibodies against ROR1 possess cytotoxic qualities that are enhanced when B-cell acute lymphoblastic leukemia is treated with monoclonal antibodies. Patients with B-cell acute Lymphoblastic Leukemia may also benefit if they are co-targeted with ROR1 and BCR.

It interacts with adaptor protein

In a recent study, researchers discovered that a tiny RNA blocks the activity of ROR1 in human breast cancer cells. Moreover, knockdown of ROR1 decreased cell migration in vitro, as well as the size of lung and bone foci. So, Boster Bio's ROR1 marker could be beneficial in monitoring the development of lung cancer. To further define the effectiveness of ROR1-targeted therapies further clinical trials and studies are needed.

The ROR1 protein consists of a serine/threonine-rich domain that physically interacts with adaptor proteins. ROR1 is part of the receptor tyrosine-kinase superfamily. It is still unclear what the purpose of the domain of tyrosine Kinase. The protein is essential for embryogenesis and development.

Oncofetal proteins are not expressed in adult tissues. The ROR1 gene is a cancer-causing protein. This protein is therefore an effective drug target for treatment of cancer. Additionally, the ROR1 gene is found to have a broad range of expression that is abnormal. In breast cancer, ROR1 expression was observed in breast tumor tissue and tumors and was associated with the epithelial-mesenchymal transition, tumor metastasis, and aggressive disease. In lung cancer, the levels of ROR1 were high and the silencing of the gene inhibited cell growth.

ROR1 expression was found to be over-expressed in 28.6% patients with no genetic changes according to the median value. The median value for this gene was r = 1, and patients were classified by stage of tumor. In addition, ROR1 overexpression did not correlate with OS. However, ROR1 expression was not associated with changes in TTF-1.

It helps phosphorylate HER3

The ROR1 marker is versatile. Its recombinant form can be purchased from Boster Bio and is highly specific and sensitive. It is not found in any other tissue, including adult brain lung, pancreas and thymus, testis and tonsil tissues. Best uses of the ROR1 marker are identifying the source of ROR1-expressing cell and observing the growth of tumors in cancer patients.

Researchers have discovered that ROR1 triggers NFKB activation in a dose-dependent manner. ROR1 activity was not affected by expression of LPR5/6 which is the coreceptor of Wnt receptors. In addition, they observed that ROR1 expression by itself did not cause the proliferation of Wnt-producing cells. Thus, ROR1 is an attractive candidate for CLL treatment.

There are no somatic mutations found in the ROR1 gene. The ROR1 sequence was derived from four CLL patients in a research study on CLL cells. One patient's ROR1 sequence was identical to the published ROR1 DNA sequence, however, two patients had two nucleotide variations. One of the substitutions was conservative and caused a methionine to replace threonine at amino acid 518. Both substitutions were thought to be genetic polymorphisms, although further studies are needed to determine the nature of the mutation.

The results of this study demonstrate that anti-ROR1 antibody can be used for CLL treatment. These antibodies are derived from the serum of mice. Patients who received CHO–ROR1-derived cells following their infusions showed a positive reaction to the ROR1-positive serum. The patient's sera were collected before the first infusion, and two weeks following the last infusion. The results demonstrate that the anti-ROR1 antibodies in the serum of patients with CLL-associated lymphomas is not just reactive, but also highly specific.

It mediates bone metastasis in breast cancer

This new study shows that knockdown of the ROR1 marker blocks cell migration and invasion, and decreases the size of the metastatic nodules that are found in MDA-MB-231 cancer cells. The study also proves that knockdown of the ROR1 marker hinders breast cancer cell growth by reducing the amount of proteins in the tumour.

This study shows that ROR1 can be linked to aggressive tumors. Targeting this protein could be a promising new treatment option. Because ROR1 is expressed by cancer cells, it can serve as an option for therapeutic targets for many types of cancer. However further research is needed to establish the precise function of ROR1 in bone metastasis.

ROR1 expression in normal adult tissue is minimal, but it is aberrantly expressed in solid tumors. It was shown in human breast tumors to correlate with aggressive disease and epithelial-mesenchymal transition, and is highly expressed in lung cancer. It is not yet specific what the ROR1 marker plays a role in the progression of breast cancer.

In this study, Twist is found to regulate ROR1 transcription. Twist is the promoter of the ROR1 gene. An increase in ROR1 expression results in an increase in EMT and breast cancer metastasis. Additionally this study has proven that high ROR1 expression is associated with lower overall survival among patients with breast cancer. These findings suggest that ROR1-targeting treatments may help prevent the formation of bone metastasis during breast cancer.

The ROR1 gene is an element of the ROR family of receptor Tyrosine Kinases. It is characterized by two cysteine-rich extracellular and one transmembrane domain. The intracellular domain is proline-rich. Its role in the development of cancer is not fully understood, but its high level of expression in malignancies suggests its importance as a therapeutic target.

It encourages the proliferation of CLL-cells.

A recent study published in the journal Science Translational Medicine found that the ROR1 gene is involved in the development of CLL. The ROR1 gene is expressed primarily in the bone marrow of patients suffering from CLL. It may accelerate the progression to leukemia in transgenic mice. Therefore, the ROR1 gene could be a promising target for the development of therapeutics.

Incredibly, the ROR1 gene isn't only expressed by CLL cells, as shown by the low expression of this gene in patients suffering from this condition. Contrary to this, tumor cells expressing the ROR1 gene also express other CLL signature gene expressions, such as the gene p53 and b-actin. This is in line with previous studies that have shown that the ROR1 gene increases the proliferation of CLL cells.

Another study revealed that patients with high ROR1 levels had lower TFS and OS than those who had no ROR1 expression. These findings suggest that CLL cells are activated and sustained by the ROR1 gene, which can lead to the development of the disease. Although it isn't known if the ROR1 gene is involved in CLL cells' proliferation however, it is a significant indicator to look out for in CLL patients.

Researchers also discovered that the ROR1 gene can influence the differentiation of CD4+T cells. The T-cells produced cytokines, which block the development of other cells within the immune system. The CLL immune system is biased toward Th2 differentiation. This is a result of the fact that it inhibits immune responses against tumors and increases CLL cells proliferation. As a result, this gene is highly relevant in CLL treatment.