Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC011307 | Panoply™ Human PARK2 Knockdown Stable Cell Line | Inquiry |
| CSC-SC011307 | Panoply™ Human PARK2 Over-expressing Stable Cell Line | Inquiry |
| CSC-RT1868 | PARK2 Knockout Cell Line-HeLa | Inquiry |
| CLKO-1720 | PARK2 KO Cell Lysate-HeLa | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD00364Z | PARK2 adenovirus | Inquiry |
| AD11815Z | Human PARK2 adenoviral particles | Inquiry |
| LV20991L | human PARK2 (NM_013988) lentivirus particles | Inquiry |
| LV20992L | human PARK2 (NM_013987) lentivirus particles | Inquiry |
| LV20993L | human PARK2 (NM_004562) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHH370728 | shRNA set against Human PARK (NM_007262.4) | Inquiry |
| SHH370732 | shRNA set against Mouse PARK (NM_020569.3) | Inquiry |
| SHH370736 | shRNA set against Rat PARK (NM_057143.1) | Inquiry |
| SHH370740 | shRNA set against Human PARK2 (NM_004562.2) | Inquiry |
| SHH370744 | shRNA set against Mouse PARK2 (NM_016694.3) | Inquiry |
| SHH370748 | shRNA set against Rat PARK2 (NM_020093.1) | Inquiry |
| SHR064644 | shRNA set against Rat Olr510_predicted(NM_001000312.1) | Inquiry |
| SHR088116 | shRNA set against Rat Park2(NM_020093.1) | Inquiry |
| SHR088320 | shRNA set against Mouse Park2(NM_016694.3) | Inquiry |
| SHW008291 | shRNA set against Danio rerio PARK2 (NM_001017635) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDCL185610 | Human PARK2 ORF clone(NM_004562.2) | Inquiry |
| CDCR252913 | Mouse Park2 ORF Clone(NM_016694.3) | Inquiry |
| CDFR011653 | Rat Park2 cDNA Clone(NM_020093.1) | Inquiry |
| MiUTR1M-08905 | PARK2 miRNA 3'UTR clone | Inquiry |
| MiUTR1R-05626 | PARK2 miRNA 3'UTR clone | Inquiry |
| CDCB169766 | Danio rerio PARK2 ORF Clone (NM_001017635) | Inquiry |
| CDCB182566 | Rabbit PARK2 ORF clone (XM_008263754.1) | Inquiry |
| CDCR378700 | Rat Park2 ORF Clone(NM_020093.1) | Inquiry |
| CDCS411853 | Human PARK2 ORF Clone (BC022014) | Inquiry |
PARK2 has some involvement in multiple signaling pathways and cellular processes as an E3 ubiquitin ligase. A RING-between-RING-type E3 ubiquitin ligase was encoded by the PARK2 gene, which is also known as PARKIN, to serve as a RING/HECT hybrid for implicating its functions in protein turnover, stress response, mitochondria homeostasis, xenophagy, metabolism, and many other cellular processes in responsible for cell growth and survival regulations. More than this, PARK2 status also has associations with risk of autosomal recessive juvenile Parkinson's disease (ARJPD), leprosy, typhoid, and paratyphoid fever. Mice with PARK2 deficiency is susceptible to tumorigenesis, PARK2 depletion makes pancreatic cancer cells more tended to proliferate and form tumors, whereas reduced growth of cancer cells of various tissue origin can be seen in ectopic PARK2. All this may suggest a tumor suppressive role of PARK2.
As one of the most common primary malignant bone tumors, osteosarcoma (OS) has a high occurrence in children and adolescents. In recent decades, PARK2 was revealed as a vital tumor suppressor gene in many malignant solid tumors. Down-regulation of PARK2 in OS tissue and cell lines has a significant association with higher tumor stage, whereas the cell cycle is arrested by overexpression of PARK2 to inhibit cell proliferation, migration, and invasion, and reduce tube formation in vitro and tumor growth and angiogenesis in vivo. A recent finding also demonstrated that the negative association between the OS growth and PARK2 gene is partially attributed to the JAK2/STAT3/VEGF signaling pathway, which is also previously been identified as a signaling regulates several important pathways in tumorigenesis, like cell cycle progression, apoptosis, tumor invasion, and metastasis. Thus, this gene may function as a therapeutic target in various human solid tumors. And the downstream protein of the JAK2/STAT3 signaling pathway, VEGF, a usually upregulated protein in multiple cancers, plays a pivotal role in angiogenesis, and its expression is in parallel with JAK2 and STAT3 expression. Inhibition on the JAK2/STAT3/VEGF signaling exerted by the PARK2 was mainly through association with other genes and protein-protein interactions. As a recent conducted study has indicated that PARK2 depletion promotes PTEN inactivation, which was found in many human cancer cell lines with the rank as the most mutated tumor suppressor gene after p53.
Figure 1. The function of parkin and PARK2-related mutations. (Shibo Ying, et al. 2021)
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