mProX™ Human HRH3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Hrh3 protein knockdown regulated cellular motility and invasion.
Cell migration was assessed using a wound-healing assay, while cell invasion was quantified through the Transwell assay. Statistical significance denoted as *P < 0.05, **P < 0.01, ***P < 0.001 in comparison to the siNC group. Images captured at ×100 and ×200 magnification.
Ref: Zhao, Yan-yan, et al. "Inhibition of histamine receptor H3 suppresses the growth and metastasis of human non-small cell lung cancer cells via inhibiting PI3K/Akt/mTOR and MEK/ERK signaling pathways and blocking EMT." Acta Pharmacologica Sinica 42.8 (2021): 1288-1297.
Pubmed: 33159174
DOI: 10.1038/s41401-020-00548-6
Research Highlights
Tian LI, et al. "Targeting LncRNA LLNLR-299G3.1 with antisense oligonucleotide inhibits malignancy ." Oncology research, 2023.
Recent studies have demonstrated the crucial involvement of long non-coding RNAs (lncRNAs) in the progression of various cancers, including esophageal squamous cell carcinoma (ESCC). However, the specific mechanisms by which lncRNAs contribute to ESCC remain unclear, making it difficult to develop effective therapies. In this research, a novel ESCC-associated lncRNA, LLNLR-299G3.1, was identified through RNA-sequencing analysis. This lncRNA was found to be up-regulated in ESCC tissues and cells, and its silencing with antisense oligonucleotides (ASOs) inhibited ESCC cell proliferation and invasion. Further investigation revealed that LLNLR-299G3.1 interacts with cancer-associated RNA binding proteins and modulates the expression of cancer-related genes, such as OSM, TNFRSF4, HRH3, and SSTR3. ChIRP-seq analysis showed that these genes contain chromatin binding sites for LLNLR-299G3.1. Rescue experiments confirmed the importance of LLNLR-299G3.1's interaction with HRH3 and TNFRSF4 in promoting ESCC cell proliferation. To target LLNLR-299G3.1 in vivo, placental chondroitin sulfate A binding peptide-coated nanoparticles loaded with ASOs (pICSA-BP-ANPs) were developed and effectively suppressed ESCC tumor growth and improved animal survival. These findings suggest that LLNLR-299G3.1 promotes ESCC progression through gene-chromatin interactions and the use of pICSA-BP-ANPs may be a promising therapeutic approach for lncRNA-associated ESCC.
Pubmed:
37415734
DOI:
10.32604/or.2023.028791
Ji Q, et al. "Genetic and neural mechanisms of sleep disorders in children with autism spectrum ." Frontiers in psychiatry, 2023.
The prevalence of sleep disorders in children with autism spectrum disorder (ASD) is high and can negatively impact development and cause challenges for families and society. The complex pathological mechanism of sleep disorders in autism may involve gene mutations and neural abnormalities. This review examines literature on the genetic and neural mechanisms of sleep disorders in children with ASD. Eligible studies published between 2013 and 2023 were identified through searches of the databases PubMed and Scopus. The literature suggests that mutations in various genes, such as MECP2, VGAT, SLC6A1, HRH1, HRH2, HRH3, KCNQ3, PCDH10, AHI1, ARHGEF10, UBE3A, SLC6A3, PTCHD1, HTR2A, SLC6A4, MAOA, MAOB, TPH2, VMATs, SHANK3, CADPS2, ASMT, MTNR1A, and MTNR1B, can affect neural circuits associated with sleep-wake regulation and lead to sleep disorders in children with ASD. Understanding these mechanisms may help inform treatment strategies for children with ASD and sleep disorders.
Pubmed:
37200906
DOI:
10.3389/fpsyt.2023.1079683