mProX™ Human SRPK3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryProduct Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
There are currently no Customer reviews or questions for mProX™ Human SRPK3 Stable Cell Line (S01YF-1023-PY15). Click the button above to contact us or submit your feedback about this product.
Alex Garcia (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Alex Johnson (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 Following treatment with srpk3 siRNA, a reduction in srpk3 expression was achieved in C2C12 cells, resulting in an observed increase in the expression levels of α-syn and phosphorylated-α-syn (p-α-syn).
The assessment of α-synuclein (α-syn) and phosphorylated-α-syn (p-α-syn) was performed through Western blot analysis subsequent to the administration of serine/arginine-rich protein specific kinase 3 (srpk3) siRNA to C2C12 cells. The Western blot assay for α-syn and p-α-syn was conducted following the application of srpk3 siRNA.
Ref: Seo, Min Hyung, and Sujung Yeo. "Srpk3 decrease associated with alpha-synuclein increase in muscles of MPTP-induced Parkinson's disease mice." International Journal of Molecular Sciences 22.17 (2021): 9375.
Pubmed: 34502283
DOI: 10.3390/ijms22179375
Research Highlights
Saaoud, Fatma. et al. "Chronic Kidney Disease Transdifferentiates Veins into a Specialized Immune-Endocrine Organ with Increased MYCN-AP1 Signaling." Cells, 2023.
The study investigated the effect of chronic kidney disease (CKD) on the transcriptome reprogramming of upper-extremity veins in patients with end-stage renal disease (ESRD) who choose hemodialysis as their treatment. Data from 48 CKD patients and 20 non-CKD controls were analyzed to identify the changes in vein gene expression. Results showed that CKD converted veins into immune organs by upregulating cytokine, chemokine, and secretome genes and increasing innate immune responses. CKD also caused impairments in mitochondrial bioenergetics and induced immunometabolic reprogramming. Additionally, fibrogenic processes and cell death and survival programs were reprogrammed, potentially priming the veins for arteriovenous fistula failure. CKD also affected protein kinase signal transduction pathways.
Saaoud, Fatma. et al. "Chronic Kidney Disease Transdifferentiates Veins into a Specialized Immune-Endocrine Organ with Increased MYCN-AP1 Signaling." Cells, 2023.
Pubmed:
37296603
DOI:
10.3390/cells12111482
Lee, Yu-Ri. et al. "Eye movement defects in KO zebrafish reveals SRPK3 as a causative gene for an X-linked intellectual disability." Research square, 2023.
Intellectual disability (ID) is a frequently-occurring neurodevelopmental condition characterized by significantly decreased intellectual and adaptive abilities. In particular, X-linked ID (XLID) disorders, resulting from defects in genes located on the X chromosome, affect 1.7 in every 1,000 males. Through the utilization of exome sequencing, the identification of three missense mutations (c.475C>G; p.H159D, c.1373C>A; p.T458N, and c.1585G>A; p.E529K) in the SET domain-containing 5 (SETD5) gene was made in three unrelated male patients with XLID.
Lee, Yu-Ri. et al. "Eye movement defects in KO zebrafish reveals SRPK3 as a causative gene for an X-linked intellectual disability." Research square, 2023.
Pubmed:
36993381
DOI:
10.21203/rs.3.rs-2683050/v1
