mProX™ Human SRPK2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Enhanced NSCLC cell proliferation is facilitated by the upregulation of SRPK2.
In CALU3 and SKMES1 cells, transfections of SRPK2 and an empty vector (Vector) were carried out. The impact of SRPK2 on in vitro cell proliferation, as assessed through BrdU staining at various time intervals, demonstrated a significant increase in SRPK2 overexpression when compared to the Vector group (all P<0.05).
Ref: Li, Xin, et al. "Downregulation of SRPK2 promotes cell cycle arrest through E2F1 in non-small cell lung cancer." European Journal of Histochemistry: EJH 63.4 (2019).
Pubmed: 31833327
DOI: 10.4081/ejh.2019.3067
Research Highlights
Cho, Sungyun. et al. "FAM120A couples SREBP-dependent transcription and splicing of lipogenesis enzymes downstream of mTORC1." Molecular cell, 2023.
The mechanistic target of rapamycin complex 1 (mTORC1) is a key regulator of cell growth, stimulating the synthesis of macromolecules through various processes, such as transcription, RNA processing, and post-translational modification of metabolic enzymes. Despite its importance, the specific mechanisms by which mTORC1 controls these gene expression programs are not fully understood. In a recent study, it was discovered that a protein known as family with sequence similarity 120A (FAM120A) acts as a co-activator of transcription, and is essential for linking mTORC1 signaling with the splicing of enzymes involved in lipid synthesis. This connection is facilitated by mTORC1-activated serine/arginine-rich protein kinase 2 (SRPK2), which phosphorylates the splicing factor serine/arginine-rich splicing factor 1 (SRSF1), enhancing its interaction with FAM120A. FAM120A, in turn, interacts directly with a key transcription factor known as SREBP1, at the promoters of active genes involved in lipid synthesis. This interaction serves to bridge the newly transcribed genes to the splicing machinery, containing SRSF1 and the RNA-splicing factor U1-70K, promoting efficient splicing and stability of the transcripts involved in fatty acid synthesis. Overall, these findings establish FAM120A as a critical co-factor in mTORC1-dependent gene regulation programs that facilitate anabolic cell growth, with implications in cancer cell proliferation.
Cho, Sungyun. et al. "FAM120A couples SREBP-dependent transcription and splicing of lipogenesis enzymes downstream of mTORC1." Molecular cell, 2023.
Pubmed:
37595559
DOI:
10.1016/j.molcel.2023.07.017
Zhou, Xianxiao. et al. "Molecular differences in brain regional vulnerability to aging between males and females." Frontiers in aging neuroscience, 2023.
The decline of cognitive function during the aging process has been linked to alterations in brain structure and a decrease in synaptic connections. Despite these findings, the specific molecular mechanisms involved in cognitive decline in normal aging are still not fully understood.
Zhou, Xianxiao. et al. "Molecular differences in brain regional vulnerability to aging between males and females." Frontiers in aging neuroscience, 2023.
Pubmed:
37284017
DOI:
10.3389/fnagi.2023.1153251
