mProX™ Human PRKD3 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1222-KX452	Magic™ Human PKD3(PRKD3 in Vitro Assay	Human		Kinase Assay

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;A2058

Target Classification

Kinase Cell Lines

Target Research Area

Cancer Research

Related Diseases

Conventional Lipoma; Prostate Cancer

Gene ID

Human:23683

UniProt ID

Human:O94806

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

PRKD3, a member of the protein kinase D (PRKD) family, has various applications in different fields. In the context of salivary gland carcinoma, PRKD3 gene fusions have been identified in the cribriform subtype of polymorphous adenocarcinoma (PAC), highlighting its potential as a diagnostic marker for this specific subtype. Additionally, PRKD3 has been implicated in heart failure, with genome-wide association studies (GWAS) and Mendelian randomization proteomics identifying it as a potential drug target for interventions in primary prevention of heart failure. In breast cancer, mutant ER-driven gene regulation is influenced by microRNAs, and PRKD3 has been found to play a role in the proliferation of ER mutant cells, suggesting its potential as a therapeutic target in breast cancer. Furthermore, PRKD3 has been shown to be involved in osteoclast formation and function, with its conditional knockout resulting in increased trabecular bone volume in male mice. Finally, in prostate cancer, PRKD3 has been identified as an isoform that is upregulated and potentially contributes to cancer progression, making it a potential target for therapeutic intervention. Overall, PRKD3 has diverse applications in cancer research, cardiovascular disease, and bone biology.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Alex Garcia (Verified Customer)

What is the role of PRKD3 in prostate cancer cell invasion and migration? Sep 12 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

PRKD3 expression is promoted by lncRNA PCA3, enhancing invasion and migration of prostate cancer cells. Sep 12 2022

chat Taylor Jones (Verified Customer)

How does PRKD3 mutation affect breast cancer cell growth? May 06 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

Mutations in estrogen receptor alpha, including those affecting PRKD3, regulate gene expression and cell growth in breast cancer through microRNAs. May 06 2020

Published Data

Fig.1 When combined with BRAF siRNA, greater growth inhibition was observed compared to any of the individual treatments when PRKD3 siRNAs were administered.

Cell viability was assessed 72 hours post-cotransfection with siRNAs targeting BRAF and PRKD3, CRAF and PRKD3, and BRAF and CRAF. Protein levels of PRKD3, BRAF, and CRAF were measured by Western blotting following siRNA transfections against PRKD3, BRAF, and CRAF, respectively. The PRKD3 protein was indicated by an arrow at the expected molecular weight, while a nonspecific band was denoted by an asterisk (*). Standard deviations were calculated from four independent experiments to represent the error bars.

Ref: Chen, Jian, et al. "Protein kinase D3 sensitizes RAF inhibitor RAF265 in melanoma cells by preventing reactivation of MAPK signaling." Cancer research 71.12 (2011): 4280-4291.

Pubmed: 21527556

DOI: 10.1158/0008-5472.CAN-10-3761

Research Highlights

Hahn, Elan. et al. "Comprehensive Molecular Characterization of Polymorphous Adenocarcinoma, Cribriform Subtype: Identifying Novel Fusions and Fusion Partners." Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2023.
In this study, the researchers aim to characterize the fusions associated with polymorphous adenocarcinoma (PAC), a common salivary gland carcinoma, through next-generation sequencing (NGS). A total of 54 PAC cases, primarily of the cribriform subtype, were identified and subjected to NGS. Of the 51 cases successfully sequenced, 28 demonstrated gene fusions involving PRKD1, PRKD2, or PRKD3, while 10 cases had the PRKD1 p.E710D mutation. A diverse group of fusion partners, including 13 novel partners, were identified, with the most common being ARID1A and ARID1B. These findings suggest the need for a wider range of sequencing approaches for confirmation of molecular diagnosis in PAC cases.
Hahn, Elan. et al. "Comprehensive Molecular Characterization of Polymorphous Adenocarcinoma, Cribriform Subtype: Identifying Novel Fusions and Fusion Partners." Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2023.
Pubmed: 37595638 DOI: 10.1016/j.modpat.2023.100305

Rasooly, Danielle. et al. "Genome-wide association analysis and Mendelian randomization proteomics identify drug targets for heart failure." Nature communications, 2023.
The authors conducted a large-scale meta-analysis of genome-wide association studies (GWAS) involving 90,000 heart failure cases and over 1 million control individuals of European ancestry. They aimed to uncover new genetic determinants for heart failure by using GWAS data and blood protein quantitative loci. Through Mendelian randomization and colocalization analyses, the authors provide evidence for the potential role of druggable proteins in the development of heart failure. They identify 39 significant heart failure risk variants, 18 of which were previously unknown. By combining Mendelian randomization proteomics and genetic cis-only colocalization, the authors identify 10 additional potential causal genes for heart failure. Ultimately, their research highlights 7 proteins (CAMK2D, PRKD1, PRKD3, MAPK3, TNFSF12, APOC3, and NAE1) that could serve as targets for interventions in primary prevention of heart failure.
Rasooly, Danielle. et al. "Genome-wide association analysis and Mendelian randomization proteomics identify drug targets for heart failure." Nature communications, 2023.
Pubmed: 37429843 DOI: 10.1038/s41467-023-39253-3