ligand  (R&D Systems)

Journal: Journal of Translational Autoimmunity

Article Title: Type I interferon-dependent and -independent signaling underlie autoantibody production in a murine lupus model

doi: 10.1016/j.jtauto.2026.100351

Figure Lengend Snippet: Induction of SLE autoantibodies occurs in the presence of LPS or Poly I:C, but not other TLR ligands. Wild type (WT) C57BL/6 mice received five immunizations with β2GPI in combination with one of the following TLR ligands: TLR2 : PAM2, FSL-1 (lipoprotein); TLR3 : Poly I:C (dsRNA); TLR4 : LPS; TLR7: IMQ (imiquimod); or TLR9 : CpG-ODN (ssDNA). Serum autoantibodies were detected by ELISA. Bars indicate the mean value +/standard error (S.E.) per group (n = 5 mice/group), and dots indicate values for individual mice. Autoantibody levels for control mice immunized with PBS and TLR ligand were OD 405 < 0.1. The OD 405 + 3 S.D. for unimmunized mice was ≤0.1 for all autoantibodies assayed. (A) Anti-β2GPI and anti-CL antibodies, and (B) hallmark SLE autoantibodies (anti-DNA, anti-Ro/SS-A, anti-La/SS-B, and anti-Sm) were analyzed statistically in separate groupings. For each of the two autoantibody categories, each different TLR ligand (immunized with β2GPI) was compared to the other TLR ligands by 2-way ANOVA, followed by a Tukey's multiple comparison test. ns = not significant. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.

Article Snippet: TLR ligands Pam2CSK4 (PAM2), FSL-1, Pam3CSK4 (PAM3), Poly I:C (HMW), imiquimod-R837 (IMQ), and CpG-ODN-1555 + 1466 (CpG-ODN) were from InvivoGen (San Diego, CA).

Techniques: Enzyme-linked Immunosorbent Assay, Control, Comparison

Journal: bioRxiv

Article Title: The importance of M1 muscarinic receptor phosphorylation in learning and memory

doi: 10.64898/2026.03.23.713145

Figure Lengend Snippet: M1-WT-HA (n=11-14) (A) , M1-KO (n=13-16) (B) or M1-PD-HA (n=11-14) (C) mice were treated with 1.5 mg/kg scopolamine +/-10 mg/kg VU846 30 mins prior to training in a fear conditioning paradigm. Mice were then returned to the same environment 24 hrs later for contextual memory retrieval whereby a reduced level of freezing indicates impaired memory. The response in vehicle treated animals across strains was also compared (D) . 2-way ANOVA with Tukey’s post-hoc correction for multiple comparisons, *p<0.05, ***p<0.001, ****p<0.0001, ns=not significant. (E ) Representative images of CA1 hippocampal region of HA-tagged M1-WT, M1-DREADD, M1-PD and M1-DREADD-PD stained with HA antibody demonstrating location of the receptor (green). Images at 40X magnification, scale bar = 50 µm

Article Snippet: The drugs utilised in this study were the pan-muscarinic antagonist, to induce a learning and memory (LM) deficit, scopolamine hydrobromide (Sigma) at 0.5-3 mg/kg doses; the M1 positive allosteric modulator (PAM) VU0486846 (VU846) at 10-100 mg/kg; and the M1-DREADD activating ligand clozapine-n-oxide (CNO) (Tocris) at 0.3 mg/kg.

Techniques: Staining

Journal: bioRxiv

Article Title: The importance of M1 muscarinic receptor phosphorylation in learning and memory

doi: 10.64898/2026.03.23.713145

Figure Lengend Snippet: (A) Male and female M1-WT-HA (n=11) and M1-PD (n=12) mice were treated with the M1-PAM VU846 30 mins prior to fear conditioning and returned to the chamber 24 hrs later for contextual memory retrieval. 2-way ANOVA ****p<0.0001 effect of strain, no significant effect of drug overall p=0.12, Bonferroni’s post-hoc correction for multiple comparisons between vehicle and VU846 for each strain, ns= not significant. (B & C) Male M1-DREADD mice were treated with 0.3 mg/kg of clozapine-N-oxide (CNO), an orthosteric agonist of the DREADD receptor, or vehicle (n=4-5 per group) 30 mins prior to training in a fear conditioning paradigm and then returned to the same environment 24 hrs later for contextual memory retrieval (B) or presentation of the tone in an altered environment 48 hrs later for cued memory retrieval (C) whereby a reduced level of freezing indicates impaired memory. (D) WT mice (n=7-9 per group) were also treated with 0.3 mg/kg CNO in a separate experiment demonstrating no effect of CNO. 2-way ANOVA with Dunnett’s post-hoc correction for multiple comparisons, ****p<0.0001, all other comparisons p>0.05.

Article Snippet: The drugs utilised in this study were the pan-muscarinic antagonist, to induce a learning and memory (LM) deficit, scopolamine hydrobromide (Sigma) at 0.5-3 mg/kg doses; the M1 positive allosteric modulator (PAM) VU0486846 (VU846) at 10-100 mg/kg; and the M1-DREADD activating ligand clozapine-n-oxide (CNO) (Tocris) at 0.3 mg/kg.

Techniques:

Journal: bioRxiv

Article Title: The importance of M1 muscarinic receptor phosphorylation in learning and memory

doi: 10.64898/2026.03.23.713145

Figure Lengend Snippet: Male M1-DREADD mice were treated with 0.01 - 0.3 mg/kg of clozapine-N-oxide (CNO), an orthosteric agonist of the DREADD receptor, or vehicle (n=5-9 per group) 30 mins prior to training in a fear conditioning paradigm and then returned to the same environment 24 hrs later for contextual memory retrieval. Data presented as freezing level normalised to the highest freezing response. One way ANOVA with Bonferroni’s post hoc correction for multiple comparisons to vehicle treatment group *p<0.05. All other comparisons not significant.

Article Snippet: The drugs utilised in this study were the pan-muscarinic antagonist, to induce a learning and memory (LM) deficit, scopolamine hydrobromide (Sigma) at 0.5-3 mg/kg doses; the M1 positive allosteric modulator (PAM) VU0486846 (VU846) at 10-100 mg/kg; and the M1-DREADD activating ligand clozapine-n-oxide (CNO) (Tocris) at 0.3 mg/kg.

Techniques: