ORAI1 Antibodies

Calcium release-activated calcium channel protein 1 (ORAI1)

Ca(2+) release-activated Ca(2+) (CRAC) channel subunit that mediates Ca(2+) influx after depletion of intracellular Ca(2+) stores and channel activation by the Ca(2+) sensor, STIM1 (PubMed:16582901, PubMed:16645049, PubMed:16733527, PubMed:16766533, PubMed:16807233, PubMed:19249086, PubMed:23307288, PubMed:24351972, PubMed:24591628, PubMed:28219928). CRAC channels are the most important pathway for Ca(2+) influx in T-cells and encourage the immune response to pathogens by activating the transcription factor NFAT (PubMed:16582901).

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Gene Information

Human
Gene Name:	ORAI1
Uniprot:	Q96D31
Entrez:	84876

Family

Belongs to:
Orai family

Alternative Names

CRACM1; CRACM1ORAT1; FLJ14466; ORAI calcium release-activated calcium modulator 1; Orai1; ORAT1; Protein orai-1; TMEM142A; TMEM142Acalcium release-activated calcium modulator 1; Transmembrane protein 142Acalcium release-activated calcium channel protein 1

Molecular Weight

Mass (kDA):
32.668 kDA

Genomic Context

Human
Location:	12q24.31
Sequence:	12; NC_000012.12 (121626550..121642040)

Subcellular Localizations

Cell membrane; Multi-pass membrane protein. Isoform beta is more mobile in the plasma membrane (PubMed:23307288). Colocalizes with STIM1 at the cell membrane (PubMed:27185316).

Diseases

• Immunologic Deficiency Syndromes
• Malignant Neoplasms
• Severe Combined Immunodeficiency
• Neoplasms
• Thrombosis
• Inflammation
• Tissue Adhesions
• Malignant Neoplasm Of Breast
• Autoimmune Diseases
• Thrombus
• Neoplasm Metastasis
• Mammary Neoplasms
• Asthma

• Congenital Combined Immunodeficiency
• Autoimmunity
• Vascular System Injuries
• Autoimmune Reaction
• Myopathy
• Hyperplasia
• Diabetes Mellitus

Interacting Proteins

• ATP2C2
• CRACR2A
• ORAI3
• STIM1
• TRPC1

• TRPC3
• Trpc6

Pathways

• Store-operated Calcium Entry
• Cell Proliferation
• Localization
• Secretion
• Lymphocyte Activation
• Rna Interference
• Cell Activation
• Cell Migration
• Immune Response
• Pathogenesis
• Platelet Activation
• T Cell Activation
• Cell Cycle

• Hemostasis
• Muscle Contraction
• Cell Death
• Exocytosis
• Mast Cell Degranulation
• Angiogenesis
• Transport

PTMs

• Phosphorylation
• Glycosylation
• Biotinylation
• Cleavage

• Reduction
• Oxidation
• Dephosphorylation
• Deglycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ORAI1

Best Uses Of The ORAI1 Marker

The ORAI1 Marker is a calcium release-activated calcium modulator that negatively regulates the TICAM1/TRIF-dependent toll-like receptor signaling pathway. This calcium-release-activated protein is also involved in macroautophagy and autophagosome formation, and is a critical component in VLP budding. This article discusses the many potential uses of ORAI1.

ORAI1 marker is a calcium release activated calcium modulator

ORAI1 is an ORM1 transmembrane-protein with a sequence containing 301 amino acid. This protein couples to a cell-cell stromal interaction molecule, which senses calcium reduction in the intracellular epiplasmic reticulum. It has 4 transmembrane domains and contains 20 and 40 amino acid residues in the first extracellular loop domain. The complete ORAI1 gene sequence can be found in the public database under Accession Nos. NM_032790 and NP_116179 (NCBI).

The protein is a membrane protein that is multi-pass and highly expressed in many tissues including the kidneys. It is also associated to immune-related diseases. Inflammatory conditions include psoriases, inflammatory bowel disorders, and autoimmune hypothyroiditis. It also interacts through its Nterminus avec ATP2C2 to regulate Ca2+ influx in the plasma membrane.

The antibody is made to inhibit Orai1s biological activity. It also inhibits CRAC channels which activate immune reactions. It can be used therapeutically in the treatment of disease that involves activation CRAC channels. This includes thrombosis or cancer. It can also treat immune-related diseases, including thrombosis and allergies, as well as thrombosis.

The ORAI1 mAb antibody has been recently developed for the treatment inflammatory bowel disorders. It works by blocking IFN-g production in human PBMC and suppressing weight loss associated with severe combined immunodeficiency mice. It also suppresses the passive cutaneous anaphylaxis response in human Orai1 knock-in mice.

ORAI1 Marker negatively regulates TICAM1/TRIF-dependent toll-like receptor signaling pathway

ORAI1 is an adaptor molecular that encodes TIR domain. It is involved intracellular signaling processes like activating nuclear factor-kappa-B, triggering the production of type I interferon b, and mediating proteins-protein interactions. The protein plays a role in many biological processes, including activating signaling pathways TLR3 or TLR4 signaling pathways.

ORAI1, which is membrane-bound, is required to autophagy. Its downregulation prevents TLR3 mediated production of IFN. The receptor is involved for immune cell regulation and the upregulation of transactivating form p63 a (TAp63a). It is therefore important in innate immunity.

Although the lncRNA is not being studied extensively, a coexpression network found relationships with six other genes in the BCC cells line. These mRNAs have been associated with mitochondrial dysfunction, glucose metabolism, and TICAM1 positively correlates with TIR-containing molecule-1.

TLR3 signals the existence of a TLR binding ligand, poly I.C. In the current study, we explored the role of miR-266a for regulation of TLR3-signaling. Using microscopic observations, we also evaluated the mRNA levels TLR3 found in the spleens PIA-treated rats treated with methotrexate. We also evaluated the effects of miR-266a inhibitors on pristaneinduced arthritis.

ORAI1 markers regulate macroautophagy.

Numerous studies have shown that cabozantinib kills aggressive, poorly-differentiated murine prostate cancer cells. Research suggests that cabozantinib promotes neutrophil recruiting and IL-8 production. It also increases angiogenesis and blood vessel permeability. There are still many questions about the role of ORAI1 for autophagosome formation.

The ORAI1 marker can be found on many cells, including immune cells as well as cancer cells. It is important in the regulation cell death and autophagy. It also inhibits IL-6 and GM-CSF accumulation. Further, the protein blocks several pathways involved with the immune system. As such, it has a broad application in autophagosome formation and maintenance.

ORAI1 inhibits FcYiRIIB and tumor immunity. This finding highlights importance of TSP-1/CD47/SIRPQia Signal Axis. This study also highlights the importance of thrombospondin-1 as a tumor immunotherapy agent. It also provides evidence for the promise of cancer vaccines.

The ORAI1 marker can be used in multiple ways in tumor immunotherapy. It has been shown to induce autophagosome formation and cytotoxicity. Its presence in tumor cells may help predict whether immunocheckpoint inhibitors will be effective. It can also be used in targeting TLR5, which suppresses tumour immunity and speeds up metastasis.

It is also a novel diagnostic marker for the detection of tumor-specific cellular immune responses. It is highly effective at detecting tumor-derived suppressor cells within lymph nodes. It also inhibits tumor induced IL-10 production, which is a key factor in tumor metastasis. ORAI1 can be used to treat tumor immunotherapy.

ORAI1 Marker is a key component of VLP budding

A study published in American Physiological Society suggests the ORAI1 marker is crucial for VLP Budding. Researchers looked at a range of cell processes, including calcium signaling. The researchers first examined how cells responded to viruses that expressed matrix proteins. Viral infection caused significant calcium changes in cell membranes. Mice lacking this gene for the calcium channel protein were unable to induce viral-induced blooming.

ORAI1 is critical for the late stages of viral budding. Inadequate levels can lead to budding. This protein is required for calcium signaling. Mutant ORAI1 protein can reduce the ability of cells infected to spread the virus. This mutation can result a hundredfold drop in VLP production. It also inhibits budding in a cell-culture model of hemorhagic disease virus.

ORAI1 plays a role in budding and cellular proliferation. It is capable of enhancing budding competence when combined with bacterial NA. The mutant HA/NA protein does not promote budding if it is missing HA. This mutant is not capable of forming VLPs. This mutant lacks the co-expressed HA/ORAI1 in WSN background.

Budding is also affected by NA. Udorn/72NA was unable to budding when there was exogenous NA. Cos-1 cells however showed the potential for gain of function. The Cos-1 cell strain is more powerful than 293T, which results in better image quality. This indicates that ORAI1 may be an essential component in VLP budding.

This technology has the potential to improve the delivery of vaccines to resource poor regions of the world. It is essential to find a stable means to produce VLP in clinical trials. In the absence of NA, ORAI1 Marker is required for VLP release and detection. EV71 VLP remains a promising candidate for vaccines.

ORAI1 Marker, a key component to ER stress due to oxidative stresses, is important

AA can develop from inflammation-induced damage of the ER. The mutation of ORAI1 can alleviate AA to some extent. There are a few complications that can occur when someone with AA has AA. To determine the best treatment, it is important that you monitor the progress of AA. The following article will examine the role of ORAI1 and its potential in ER Stress by Oxidative Stress.

The suppressive effect resveratrol has on SOCE in vitro can be reversed by overexpression ORAI1. The 200 mM resveratrol compound exerts a powerful suppressive effect on SOCE. This study involved 48-hour treatment with resveratrol compound 200 mM followed by calcium imaging. The calcium levels of SOCE as well as ER calcium stores were depleted. There was no difference in the calcium levels.

Activation of ORAI1 suppresses the effects of apoptosis and ER stress in mice fed a high-fat diet. SalB treatment, however, suppressed ER stress in HK2 cells and apoptosis. Furthermore, SalB failed to suppress TG-induced ER stress. However, this drug could play a role in preventing ER injury from obesity.

This discovery also opens the door to new therapeutic avenues. These results suggest a new method to prevent irregular heartbeats. In addition, Liu et al. found that oxidative stress induces the production of a protein called kinase C. These factors are involved in ischemic hearts. Therefore, regulating the activity of ORAI1 may be useful in treating this disease.