mProX™ Human MERTK Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Effects of MERTK knockdown on cell growth.
A colorimetric assay was used to assess the proliferation of OCI/AML5 and TMD7 cells transfected with 40 nM of siRNA against MERTK after 3 and 5 days, respectively. The data are shown as a percentage of the mean optical density of MERTK-knockdown cells normalized to that of vector control cells. *Statistically significant difference at p0.05 versus control
Ref: Koda, Yuki, Mai Itoh, and Shuji Tohda. "Effects of MERTK inhibitors UNC569 and UNC1062 on the growth of acute myeloid Leukaemia cells." Anticancer research 38.1 (2018): 199-204.
Pubmed: 29277773
DOI: 10.21873/anticanres.12208
Research Highlights
E, Christy; F, Nicholas. "Macrophages make a difference in cholestatic liver diseases - but how?" Journal of hepatology, 2023.
The article is an editorial that discusses how macrophages, immune cells that accumulate around bile ducts, contribute to inflammation and fibrosis in cholestatic liver diseases such as PBC and PSC. It focuses on how a transcription factor called ARID3A inhibits a receptor called MERTK, which mediates macrophage clearance of apoptotic cells (efferocytosis). The article suggests that targeting ARID3A to enhance macrophage efferocytosis may be a novel way to ameliorate liver injury and promote liver repair.
E, Christy; F, Nicholas. "Macrophages make a difference in cholestatic liver diseases - but how?" Journal of hepatology, 2023.
Pubmed:
37821021
DOI:
10.1016/j.jhep.2023.09.022
Sasaki, Takahiro. et al. "Progranulin deficiency exacerbates cardiac remodeling after myocardial infarction." FASEB bioAdvances, 2023.
Myocardial infarction (MI) is a fatal disease that results in irreversible damage to heart muscle cells and subsequent cardiac changes. Previous studies have demonstrated the protective effects of recombinant progranulin (PGRN) against myocardial ischemia and reperfusion injury. However, the role of PGRN in post-MI remains unclear. In this study, the effects of PGRN deficiency on cardiac remodeling after MI were investigated by analyzing histology and protein expression in both wild-type and PGRN-knockout mice. The results showed that PGRN expression increased in the heart, particularly in the border areas, in the days following MI. Conversely, PGRN-knockout mice exhibited higher mortality rates, increased fibrosis in the left ventricle, and more severe arrhythmia after MI. PGRN-knockout also led to an increase in levels of CD206 and MerTK expression, as well as macrophage infiltration in the myocardium, attributed to a larger subpopulation of CCR2+ and non-CCR2+ macrophages. To further understand this process, bone marrow-derived macrophages (BMDMs) were treated with LPS,Äâ+,ÄâIFN-Œ≥ and IL-4 to assess mRNA levels and phagocytic abilities. These findings suggest a role for PGRN in modulating post-MI cardiac remodeling.
Sasaki, Takahiro. et al. "Progranulin deficiency exacerbates cardiac remodeling after myocardial infarction." FASEB bioAdvances, 2023.
Pubmed:
37810172
DOI:
10.1096/fba.2023-00084
