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rfp tag  (Proteintech)


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    Proteintech rfp tag
    Rfp Tag, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 105 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rfp tag/product/Proteintech
    Average 94 stars, based on 105 article reviews
    rfp tag - by Bioz Stars, 2026-02
    94/100 stars

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    The ability of PDE11Ai’s to reverse PDE11A4 LLPS was unaffected by A) preventing phosphorylation at S163, or B) preventing phosphorylation of at S239. Although introducing the A499D mutation that stabilizes PDE11A4 homodimerization did not completely block the ability of C) BC11-38 and D) SMQ-02-57 to reduce PDE11A4 LLPS, E) it did reduce the effectiveness of PDE11Ai’s across 6 experiments. F) Further, the ability of the A499D mutant to increase PDE11A4 LLPS in this series was ∼3-fold greater in the inhibitor-treated vs. vehicle-treated cells. Next we assessed the therapeutic potential PDE11Ai’s by determining if they could reverse the increased PDE11A4 LLPS caused by G) the aging-related S117D/S124D mutant,H) staurosporine, or the overexpression of the trans-Golgi network proteins I) TGN-38 (a.k.a. TGOLN1) and J) <t>RhoB.</t> In each experiment, PDE11Ai’s completely blocked the effects of the pro-LLPS manipulations. Post hoc: *vs. vehicle, P=0.0145-0.0001; #vs. WT, mCherry, or 0 µM staurosporine, P=0.0465-0.0001.
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    The ability of PDE11Ai’s to reverse PDE11A4 LLPS was unaffected by A) preventing phosphorylation at S163, or B) preventing phosphorylation of at S239. Although introducing the A499D mutation that stabilizes PDE11A4 homodimerization did not completely block the ability of C) BC11-38 and D) SMQ-02-57 to reduce PDE11A4 LLPS, E) it did reduce the effectiveness of PDE11Ai’s across 6 experiments. F) Further, the ability of the A499D mutant to increase PDE11A4 LLPS in this series was ∼3-fold greater in the inhibitor-treated vs. vehicle-treated cells. Next we assessed the therapeutic potential PDE11Ai’s by determining if they could reverse the increased PDE11A4 LLPS caused by G) the aging-related S117D/S124D mutant,H) staurosporine, or the overexpression of the trans-Golgi network proteins I) TGN-38 (a.k.a. TGOLN1) and J) RhoB. In each experiment, PDE11Ai’s completely blocked the effects of the pro-LLPS manipulations. Post hoc: *vs. vehicle, P=0.0145-0.0001; #vs. WT, mCherry, or 0 µM staurosporine, P=0.0465-0.0001.

    Journal: bioRxiv

    Article Title: Molecular mechanisms regulating PDE11A4 age-related liquid-liquid phase separation (LLPS) and its reversal by selective, potent and orally-available PDE11A4 small molecule inhibitors both in vitro and in vivo

    doi: 10.1101/2025.05.20.654583

    Figure Lengend Snippet: The ability of PDE11Ai’s to reverse PDE11A4 LLPS was unaffected by A) preventing phosphorylation at S163, or B) preventing phosphorylation of at S239. Although introducing the A499D mutation that stabilizes PDE11A4 homodimerization did not completely block the ability of C) BC11-38 and D) SMQ-02-57 to reduce PDE11A4 LLPS, E) it did reduce the effectiveness of PDE11Ai’s across 6 experiments. F) Further, the ability of the A499D mutant to increase PDE11A4 LLPS in this series was ∼3-fold greater in the inhibitor-treated vs. vehicle-treated cells. Next we assessed the therapeutic potential PDE11Ai’s by determining if they could reverse the increased PDE11A4 LLPS caused by G) the aging-related S117D/S124D mutant,H) staurosporine, or the overexpression of the trans-Golgi network proteins I) TGN-38 (a.k.a. TGOLN1) and J) RhoB. In each experiment, PDE11Ai’s completely blocked the effects of the pro-LLPS manipulations. Post hoc: *vs. vehicle, P=0.0145-0.0001; #vs. WT, mCherry, or 0 µM staurosporine, P=0.0465-0.0001.

    Article Snippet: RFP-tagged Rhob (Cat# RC100059) and RFP-tagged TGOLN/TGN38 plasmids (Cat# RC100061) were obtained from OriGene.

    Techniques: Phospho-proteomics, Mutagenesis, Blocking Assay, Over Expression