PRCC KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon 1 and 186 bp deletion in exon 1.
PRCC_HUMAN, Papillary renal cell carcinoma (Translocation associated), isoform CRA_b, Papillary renal cell carcinoma translocation-associated gene protein, Proline-rich protein PRCC, RCCP1, TPRC
PRCC KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon 1 and 186 bp deletion in exon 1.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.
Papillary renal cell carcinoma (PRCC) also known as papillary renal is a significant variant of kidney cancer. It arises mechanically from the epithelial cells of the kidney tubules that exhibit papillary growth patterns. PRCC lacks a single protein target but involves various changes on the molecular level often linked to genetic alterations such as mutations in the MET oncogene. These changes can affect cell surface expression and signal pathways. The mass or size data about individual protein targets in this context is not typically described due to the complex and multi-genetic nature of PRCC.
PRCC forms as a type of cancer characterized by the formation of finger-like projections in the kidney. It does not align to a single protein or simple biological function but involves components like alterations in the MET pathway an independent complex soliciting increased proliferative and migratory signals within renal tissues. This process can lead to the unusual cell growth that distinguishes PRCC in affected kidneys.
MET signaling pathway and the associated HGF (hepatocyte growth factor) signaling cascade are closely involved in papillary renal phenotypes. These pathways contribute significantly to cell growth migration and differentiation regulation within the renal system. It's related to proteins such as RAS and PI3K which play essential roles in further amplifying cellular signals that contribute to oncogenesis.
PRCC is closely linked to kidney cancer specifically identified in renal cell carcinoma spectrum. Genetic evidence connects PRCC to von Hippel-Lindau (VHL) disease a disorder known to predispose individuals to various tumors. The VHL protein exhibits abnormal function in both VHL disease and PRCC highlighting its role in disease progression and potential as a therapeutic target. Additionally the involvement of the MET protein stands out as a specific player in familial cases of PRCC contributing to an inherited predisposition to this type of cancer.
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Terms & Conditions.
Allele-1: 13 bp deletion in exon1
Allele-2: 186 bp deletion in exon 1.
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