mProX™ Human CALCR Stable Cell Line

Product Information

Target Protein

CALCR

Target Family

Calcitonin Family

Target Protein Species

Human

Host Cell Type

LN229;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

Metabolic Research

Related Diseases

Osteoporosis;Bone Mineral Density Quantitative Trait Locus 15

Gene ID

Human: 799

UniProt ID

Human: P30988

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

The Calcitonin Receptor (CALCR) has been a subject of extensive research, particularly in the context of calcium homeostasis and bone metabolism. This receptor is known to mediate the effects of calcitonin, a hormone that plays a pivotal role in regulating calcium levels in the blood. Scientific studies have delved into the mechanisms by which CALCR influences bone resorption, highlighting its potential as a therapeutic target for osteoporosis and other bone-related disorders. Furthermore, recent research has unveiled the role of CALCR in the regulation of feeding behavior, emphasizing its significance in energy homeostasis. The intricate interplay between CALCR and various neuropeptides, such as adrenomedullin, has also been a focal point, revealing its multifaceted role in physiological processes. Additionally, the genetic variations associated with CALCR have been explored to understand their implications in disease susceptibility and drug responsiveness. Overall, the application of CALCR in scientific research offers promising avenues for therapeutic interventions and a deeper understanding of calcium regulation in the body.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Jessica (Verified Customer)

Are there any specific cell lines associated with CALCR research? Sep 26 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

Yes, research has been conducted using specific cell lines to understand the role and impact of CALCR in various cellular processes. Sep 26 2022

chat Deborah (Verified Customer)

How does CALCR influence cellular signaling pathways? Apr 27 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

CALCR can activate specific signaling pathways, leading to various cellular responses, including cell proliferation, migration, and adhesion. Apr 27 2021

Published Data

Fig.1 Colony suppression assay in LN229/VC and LN229/CALCR stable cells transfected with shRAMP1.

Calcitonin effectively suppressed cellular functions in both shNT and shRAMP1 settings of LN229/VC, with a heightened inhibitory effect observed in LN229/CALCR cells, albeit comparable between shNT and shRAMP1 conditions.

Ref: Pal, Jagriti, et al. "Loss-of-function mutations in calcitonin receptor (CALCR) identify highly aggressive glioblastoma with poor outcome." Clinical Cancer Research 24.6 (2018): 1448-1458.

Pubmed: 29263181

DOI: 10.1158/1078-0432.CCR-17-1901

Research Highlights

Yeom J, et al. "Surface proteins of Propionibacterium freudenreichii MJ2 inhibit RANKL-induced ." Scientific reports, 2023.
The effect of the dairy bacterium Propionibacterium freudenreichii MJ2 (MJ2) on osteoclast differentiation and its mechanism were investigated. A study was conducted using the murine macrophage cell line RAW 264.7 to evaluate the inhibitory effect of the surface proteins of MJ2 on receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclast differentiation. Results showed that the surface proteins significantly inhibited osteoclast differentiation in a dose-dependent manner. This was achieved through the downregulation of genes and proteins related to osteoclast differentiation, as well as through the upregulation of lipocalin-2 (lcn2) expression. Silencing of lcn2 through siRNA decreased the inhibitory effect of the surface proteins, indicating its importance in the inhibition of osteoclast differentiation. In conclusion, the surface proteins of MJ2 show an inhibitory effect on osteoclast differentiation by upregulating lcn2 expression, which in turn downregulates NFATc1 and its downstream genes, thus inhibiting osteoclastogenesis.
Pubmed: 37730858 DOI: 10.1038/s41598-023-42944-y

Wang Q, et al. "Anti-osteoporosis mechanism of resistance exercise in ovariectomized rats based ." Frontiers in endocrinology, 2023.
Postmenopausal osteoporosis is a leading cause of fractures among women. However, the underlying mechanism of how resistance exercise improves bone mineral density in these patients is unknown. This study aimed to uncover the mechanisms behind resistance exercise in improving osteoporosis in rats using transcriptome sequencing. Eighteen female Sprague-Dawley rats were divided into three groups - sham-operated, non-exercise, and resistance exercise - with ovariectomy performed to simulate postmenopausal osteoporosis. The resistance exercise group underwent two weeks of adaptive training and 12 weeks of resistance exercise, 5 days a week. Results showed that resistance exercise effectively counteracted the weight gain in ovariectomized rats and improved bone mineral density and trabecular bone microarchitecture. RNA-seq and enrichment analysis revealed that regulation of gene expression and osteoclast differentiation were the most closely related biological process and signaling pathway in both exercise and non-exercise groups. Further analysis through Elisa and RT-qPCR showed that resistance exercise inhibits osteoclast activation and prevents enhanced bone resorption by regulating Fos/Fosb and Calcr pathways. This study highlights the potential of resistance exercise in preventing bone loss in postmenopausal osteoporosis patients.
Pubmed: 37664852 DOI: 10.3389/fendo.2023.1162415