Journal: The Journal of Neuroscience

Article Title: Blocking Synaptic Removal of GluA2-Containing AMPA Receptors Prevents the Natural Forgetting of Long-Term Memories

doi: 10.1523/JNEUROSCI.3333-15.2016

Figure Lengend Snippet: Cannula placements. A, Figure 1D–F (white circles: Ctrl; black circles: GluA23Y). B, Figure 2A–C (white circles: Ctrl; black circles: G2CT). C, Figure 2D–F (white circles: Ctrl; black circles: GluA23Y). D, Figure 3A–C (white circles: PI; black circles: RI). E, Figure 3D–F (white circles: Ctrl; black circles GluA23Y). F, Figure 4D–F (white circles: Ctrl; black circles GluA23Y). G, Figure 5D–F (white circles: Ctrl; black circles GluA23Y). H, Figure 6A–C (white circles: Ctrl; black circles GluA23Y).

Article Snippet: The peptides G2CT and inactive control G2CT variant were purchased from AnaSpec.

Techniques:

Journal: The Journal of Neuroscience

Article Title: Blocking Synaptic Removal of GluA2-Containing AMPA Receptors Prevents the Natural Forgetting of Long-Term Memories

doi: 10.1523/JNEUROSCI.3333-15.2016

Figure Lengend Snippet: Interfering with AP2-dependent GluA2/AMPAR removal and delayed onset of GluA23Y infusions prevent forgetting of long-term object location memories. A–C, Inhibiting AP2-dependent synaptic removal of GluA2/AMPARs prevents forgetting (see Fig. 8B for cannula placements). A, Animals were trained as before (Fig. 1D), but instead of GluA23Y, the peptide G2CT (n = 7, inactive control peptide, Ctrl, n = 7) was infused to interfere with the binding of AP2 to GluA2 to attenuate activity-dependent synaptic removal of GluA2/AMPARs. B, Only animals infused with G2CT preferred exploring the object at the new location, expressing significantly stronger novelty preference than the animals infused with the inactive control peptide (Ctrl). C, There were no group differences in exploratory activity. D–F, Infusing GluA23Y can prolong remote memories shortly before they would be naturally forgotten (see Fig. 8C for cannula placements). D, Seven days after the last training session (i.e., on day 8 after training), shortly before rats normally would forget the location memory (see Fig. 1A–C), animals received GluA23Y infusions into the dorsal hippocampus twice daily for 6 d. Twenty-four hours after the last infusion (or 14 d after the end of training), memory for object location was assessed by moving one of the objects to a novel location. E, Animals infused with GluA23Y (n = 7) preferred to explore the object at the new location, whereas animals that had received the inactive control variant (Ctrl, n = 6) explored both objects for an equal amount of time. The group difference was significant. F, Exploratory activity was the same for both groups.

Article Snippet: The peptides G2CT and inactive control G2CT variant were purchased from AnaSpec.

Techniques: Binding Assay, Activity Assay, Expressing, Variant Assay

Journal: The Journal of Neuroscience

Article Title: Blocking Synaptic Removal of GluA2-Containing AMPA Receptors Prevents the Natural Forgetting of Long-Term Memories

doi: 10.1523/JNEUROSCI.3333-15.2016

Figure Lengend Snippet: Exploratory behavior during training sessions

Article Snippet: The peptides G2CT and inactive control G2CT variant were purchased from AnaSpec.

Techniques:

Journal: HemaSphere

Article Title: Myb overexpression synergizes with the loss of Pten and is a dependency factor and therapeutic target in T‐cell lymphoblastic leukemia

doi: 10.1002/hem3.51

Figure Lengend Snippet: Peptidomimetic blockade of MYB triggers cell death in T‐ALL. (A, B) Line chart of the ratio of luminescence detected using CellTiter‐Glo cell viability assay (hereafter called relative viability) upon treatment of cell lines with 10–40 µM of MYBMIM (colored line) or its inactive version, named TG3 (black line), normalized to the untreated condition. (A) MyPL1 and MyPL2 are murine R26‐Myb tg/tg ; Pten fl/fl ; Lck‐Cre tg/+ T‐ALL cell lines. (B) RPMI‐8402, P12‐Ichikawa, Loucy, KOPT‐K1, and Jurkat are human T‐ALL cell lines. (C) Bar chart showing the relative viability of Jurkat and KOPT‐K1 cells at the beginning of the experiment (0 h), and 48 h later, when treated with either 30 µM (for Jurkat) or 20 µM (for KOPT‐K1) of MYBMIM, TG3, or untreated (CTR 48 h). (D) Stacked bar charts showing the percentage of cells per phase of the cell cycle and (E) the percentage of viable, early apoptotic, or late apoptotic cells at 48 h. A representative result from two independent experiments is shown. (F) Scheme of generation of T‐ALL patient‐derived xenografts (PDXs) through intravenous injections, followed by their ex vivo treatment with either TG3 or MYBMIM. (G) Line chart of the relative viability of T‐ALL PDX with either chromosomal translocation ( TRB::MYB ), genomic gain of MYB ( MYB CNG), or wild‐type MYB ( MYB WT), upon treatment with 10–40 µM of MYBMIM (colored line) or TG3 (black line), normalized to the untreated condition.

Article Snippet: Murine and human T‐ALL cells were cultured at a density of 10,000 cells/mL and treated with either the peptidomimetic MYBMIM or the inactive control peptide TG3, which were synthetized by LifeTein.

Techniques: Viability Assay, Derivative Assay, Ex Vivo, Translocation Assay