mProX™ Human DRD1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR 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 DRD1 Stable Cell Line (S01YF-0923-PY59). Click the button above to contact us or submit your feedback about this product.
Kimberly (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Donna (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 DRD1 inhibits inflammation in DOX-treated H9C2 cells.
In the assessment of IL-1β levels within the culture supernatants of H9C2 cells treated with DOX and A-68930 following DRD1 knockdown, ELISA analysis was conducted, with a sample size of n = 4. Statistical significance (∗p < 0.05) was observed. The data is expressed as the mean ± SEM.
Ref: Liu, Jiao, et al. "Dopamine D1 receptor alleviates doxorubicin-induced cardiac injury by inhibiting NLRP3 inflammasome." Biochemical and Biophysical Research Communications 561 (2021): 7-13.
Pubmed: 33992835
DOI: 10.1016/j.bbrc.2021.04.098
Research Highlights
Yi L, et al. "Cotransplantation of NSCs and ethyl stearate promotes synaptic plasticity in PD ." Journal of ethnopharmacology, 2023.
Traditional Chinese medicine considers kidney deficiency to be a major causative factor in the development of Parkinson's disease (PD), a neurodegenerative disorder closely associated with aging. In the clinic, PD patients are often treated with Testudinis Carapax et Plastrum (Plastrum Testudinis, PT), a traditional Chinese herbal remedy that tonifies the kidney. Previous research has shown that ethyl stearate (PubChem CID: 8122), an active compound in Plastrum Testudinis Extracted with ethyl acetate (PTE), can promote the differentiation of neural stem cells (NSCs) into dopaminergic (DAergic) neurons. However, the efficacy and mechanism of cotransplantation of ethyl stearate and NSCs in treating PD model rats require further investigation. The aim of this study is to examine the use of cotransplantation therapy with NSCs and ethyl stearate in PD model rats and its effect on synaptic plasticity. Behavioral tests and molecular analyses were used to evaluate the therapeutic outcome of ethyl stearate in combination with NSCs transplantation therapy in reducing motor dysfunction, restoring dopamine levels, and improving synaptic plasticity in PD model rats. The results suggest that this cotransplantation therapy has potential as a therapeutic strategy for PD treatment.
Pubmed:
37806537
DOI:
10.1016/j.jep.2023.117292
Diepenbroek C, et al. "Dopamine in the nucleus accumbens shell controls systemic glucose metabolism via ." Metabolism: clinical and experimental, 2023.
Recent research suggests that the striatal dopamine system plays a crucial role in regulating glucose metabolism. In particular, treatment with dopamine antagonists has been associated with insulin resistance and hyperglycemia, while dopamine agonists are used to treat type 2 diabetes mellitus. However, the exact mechanism underlying the effects of striatal dopamine on glucose metabolism is not fully understood. In this study, the authors used various methods to investigate the role of dopamine signaling in the nucleus accumbens shell (sNAc) in glucose metabolism. They found that infusion of vanoxerine (a dopamine reuptake inhibitor) into the sNAc reduced endogenous glucose production and increased vagal activity, and that sNAc neurons directly targeted glutamatergic cells in the lateral hypothalamic area (LHA). Additionally, the effect of sNAc-VNX on glucose metabolism was dependent on GABAergic signaling in the LHA and intact hepatic vagal innervation. These findings suggest that striatal dopamine signaling modulates glucose metabolism through a sNAc-LHA-liver axis, and may shed light on the effects of dopamine-related medications on glucose regulation.
Pubmed:
37804881
DOI:
10.1016/j.metabol.2023.155696