anti nogo a antibody drug substance  (Novartis)

Journal: bioRxiv

Article Title: Leishmania exploits the macrophage endoplasmic reticulum-shaping protein CLIMP-63 to modulate mitochondrial biogenesis and bioenergetics

doi: 10.64898/2026.03.19.712868

Figure Lengend Snippet: BMM (treated with siRNA to either CLIMP-63 or RTN4 or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.

Article Snippet: The mouse anti-CLIMP-63 monoclonal antibody (sc-393544) was from Santa Cruz Biotechnology, the rabbit anti-RTN4 polyclonal antibody (ab186735) and the rat anti-BrdU (ab6326) were from Abcam, the rabbit polyclonal antibody RTN4 (10950-1-AP) was from Proteintech, the mouse anti-phosphoglycan (Galβ1,4Manα1-PO4) CA7AE monoclonal antibody ( ) was from Cedarlane, the rabbit anti-β-actin polyclonal antibody was from Cell Signalling, the rabbit anti-Tom20 polyclonal antibody (EPR15581-54) was from Abcam, and the rat anti-LAMP-1 monoclonal antibody 1D4B developed by J.T.

Techniques: Control, Infection, Comparison

Journal: Frontiers in Systems Neuroscience

Article Title: Is there a correlation between functional recovery of manual dexterity after motor cortex lesion and initial motor learning slope in the intact state?

doi: 10.3389/fnsys.2026.1754760

Figure Lengend Snippet: Two hypotheses to be tested. (A) Cartoon illustrating the typical time course of manual dexterity score for an adult “untreated” macaque monkey (“monkey a”), based on the modified Brinkman Board task executed with the dominant hand, including the initial motor learning phase, with a steep learning curve slope (“Ln. Sl. a”). The end of the learning phase is characterized by a plateau. Then, a unilateral experimental M1 lesion contralateral to the tested hand took place (purple vertical line), which provoked a total loss of manual dexterity during a few weeks. It was followed by a spontaneous, progressive functional recovery, until reaching a single plateau of recovery. The dashed line represents the corresponding recovery curve slope (“Rc. Sl. a”). In absence of treatment, the plateau remained stable for months to years. The vertical arrow represents the recovered post-lesion score. (B) Same as in panel (A) , but for a gentle learning curve slope represented by an untreated “monkey b.” Note that both slopes ( learning curve slope and recovery curve slope ) are clearly less steep than for “monkey a.” Seven monkeys included in the present study corresponded to such a time course, as depicted in panels (A,B) , with various learning and recovery curve slopes . The hypothesis 1 tested in the present report argues that the initial motor learning slope is correlated with the slope of functional recovery from a M1 lesion, possibly following the relationship between learning curve slope and recovery curve slope as depicted in panel (D) . As a consequence, the hypothesis 2 argues that in case of “steep initial motor learning” a higher recovered score of manual dexterity after M1 lesion will be reached than in case of “gentle initial motor learning.” (C) Same as in panels (A,B) , but for a M1 lesioned monkey subjected to a treatment (either anti-Nogo-A antibody or ANCE autologous cellular therapy; n = 6 monkeys). The M1 lesion is indicated by the vertical purple line, followed by the treatment onset (red arrow pointing down). Following the total loss of manual dexterity, a first plateau of functional recovery took place, reflecting an initial spontaneous recovery. This first plateau of recovery was used to derive six additional data points to the seven data points illustrated in panels (A,B) . Overall, 13 data points were representative of the spontaneous recovery post-M1 lesion [ ; see also for more detail]. As a result of treatment, these six monkeys exhibited a second plateau of functional recovery, representing the effect of the treatment (red curve). As for the first plateau, a recovery curve slope (“Rc. Sl.”) and a recovery score (red arrow pointing up) can be derived specifically for the second plateau , corresponding overall to six “treatment” data points. (D) Expected correlation between the recovery curve slope and the initial learning curve slope , for both plateau 1 and plateau 2 (see above).

Article Snippet: The author declares that the anti-Nogo-A antibody used in this study was provided by Novartis AG.

Techniques: Modification, Functional Assay, Gentle, Derivative Assay