Target cells specifically using cell-surface markers
Come visit us at The Society for Neuroscience in Chicago – October 19-23, Booth #763. We have some exciting new products to talk to you about.
The Society for Neuroscience meeting is just around the corner. Come visit us in Chicago – October 19-23, Booth #763.
Here are a list of the posters competing for the Annual Post of the Year Award using ATS products. (click to zoom)
Fab-pHast products bind to your primary antibody via a secondary antibody or Streptavidin cross-linked to a pH-dependent fluorescent reporter. This fluorescent reporter increases intensity as the pH of its surroundings becomes more acidic, as evident when exposed to the environment inside a cell.
SLC46A3 as a Potential Predictive Biomarker for Antibody-Drug Conjugates Bearing Noncleavable Linked Maytansinoid and Pyrrolobenzodiazepine Warheads.
Kinneer K, et al. Clin Cancer Res, 24 (24):6570-6582, 2018.
Objective: To develop biomarkers to uncover the underlying mechanism of resistance by certain cell lines for ADCs.
Summary: Loss of SLC46A3 expression was found to be a mechanism of innate and acquired resistance to ADCs bearing DM1 and SG3376.
Dose: For Lysosomal trafficking, ADCs were labeled with Fab-pHast human (Cat. #PH-01). Cells were incubated with 3 mg/mL of labeled ADCs at 37°C for desired time points and fluorescence quantified by flow cytometry.
pHast Ab Internalization Assay
Parental HEK-293 cells, and HEK-293 cells transfected with the p75 receptor, were plated in a 96-well plate overnight. Titrated 192-IgG antibody (Cat. #AB-N43) was incubated at RT with 50 nM of Fab-pHast Mouse (Cat. PH-02) for 20 min prior to addition to cells. Plates were incubated overnight to allow maximum internalization, but a few hours is sufficient for detection.
Please let us know if we can answer any questions about this promotion or any of our products.
Screen your antibodies for binding and internalization in less than 24 hours with the next generation of high throughput antibody screening.
Fab-pHast is available for mouse and human antibody screening
Fab-pHast mouse (PH-02) and/or Fab-pHast human (PH-01).
NEW: Streptavidin-pHast (PH-03) works with your biotinylated antibody.
Use promo code pHASTscreen when placing your ONLINE ORDER and save 30% on your Fab-pHast order!
Expires 31 December, 2019
Please let us know if we can answer any questions about this promotion or any of our products.
Discovery and Development of N-[4-(1-Cyclobutylpiperidin-4-Yloxy)Phenyl]-2-(Morpholin-4-Yl)Acetamide Dihydrochloride (Suvn-G3031): A Novel, Potent, Selective, and Orally Active Histamine H3 Receptor Inverse Agonist with Robust Wake-Promoting Activity. (2019). J Med Chem, 62 (3):1203-1217. Nirogi R, Shinde A, Mohammed AR, Badange RK, Reballi V, Bandyala TR, Saraf SK, Bojja K, Manchineella S, Achanta PK, Kandukuri KK, Subramanian R, Benade V, Palacharla RC, Jayarajan P, Pandey S, & Jasti V.
Objective: To examine the effects of clinical candidate, 17v on sleep/wake activity in Orexin-SAP lesioned male Wistar rats.
Summary: 17v demonstrated high receptor occupancy and marked wake-promoting effects with decreased rapid-eye-movement sleep in Orexin-SAP lesioned rats supporting its potential therapeutic utility in treating human sleep disorders.
Dose: Intracerebral injections of Orexin-SAP (100 ng/0.5 μl) in lateral hypothalamus of rats produce selective disruption of neurons containing orexin-B receptors and produces symptoms that are characteristic of narcolepsy.
Leptin receptor-expressing neurons in the ventromedial nucleus of the hypothalamus contribute to weight loss caused by fourth ventricle leptin infusions. (2019). Am J Physiol Endocrinol Metab PMID: 31361549
Seamon M, Ahn W, Li A-J, Ritter S, & Harris RBS.
Objective: To test the importance of VMH leptin responsiveness in mediating weight loss caused by fourth ventricle leptin infusion.
Summary: Leptin did not inhibit food intake and respiratory exchange ratio in rats treated with Leptin-SAP. VMH leptin receptors do not play a significant role in maintaining energy balance in basal conditions, but limit weight gain during positive energy balance.
Dose: Bilateral VMH 75-nl injections of 260 ng/ml of Leptin-SAP or Blank-SAP.
This collection of targeted toxins is useful in studying various aspects of satiety, appetite, and metabolism. Order individual conjugates in larger sizes once you’ve found the one that works best for your application.
The kit includes 10-microgram aliquots of three targeted toxins: NPY-SAP (Cat. #IT-28), Oxytocin-SAP (Cat. #IT-46), and Leptin-SAP (Cat. #IT-47). These conjugates are all expected to react in rat and mouse.
Each targeted toxin specifically eliminates cells that recognize and internalize the respective peptides: Neuropeptide Y, Oxytocin, or Leptin.
Unconjugated Saporin (25 micrograms) is included as Control.
Neuroprotective Effects of Exercise on the Morphology of Somatic Motoneurons Following the Death of Neighboring Motoneurons. (2019). Chew C, & Sengelaub DR. Neurorehabil Neural Repair, epub ahead of print 1545968319860485.
Objective: To explore whether exercise shows the same neuroprotective effect on induced dendritic atrophy as that seen with androgen treatment.
Summary: Exercise following neural injury exerts a protective effect on motoneuron dendrites comparable to that seen with exogenous androgen treatment.
Dose: Motoneurons innervating the left vastus medialis muscle were selectively killed by intramuscular injection of CTB-SAP (2 μL, 0.1%). Saporin injection reduced the weight of the vastus medialis muscle; exercise had no effect on muscle weight.
Spinal Neuropeptide Y1 Receptor-Expressing Neurons Form an Essential Excitatory Pathway for Mechanical Itch. (2019). Cell Reports, 28 (3):625-639.e626. Acton D, Ren X, Di Costanzo S, Dalet A, Bourane S, Bertocchi I, Eva C, & Goulding M.
Objective: To determine the central pathway for mechanical itch.
Summary: NPY-Y1 signaling regulates the transmission of innocuous tactile information by establishing biologically relevant thresholds for touch discrimination and mechanical itch reflexes. neither the evoked nor spontaneous scratching seen following activation of Y1Cre neurons was affected by ablation of the GRPR+ neurons. NK1R+ neuron ablation failed to modulate mechanically evoked itch.
Dose: P28 mice were given a single intrathecal (i.t.) injection of either Bombesin-SAP (400 ng in 5 mL 0.9% sterile saline) to ablate GRPR+ cells or SSP-SAP to ablate NK1r+ neurons (100 ng in 5 mL 0.9% sterile saline). Littermate controls received Blank-SAP (equal mass in 5 mL 0.9% sterile saline).
Also see:
Cross-Talk between Distinct Receptors Shapes Itch Behavior in the Spinal Cord (September 14, 2018). Available at http://dx.doi.org/10.2139/ssrn.3249822. Meng, Qing-Tao et al.
Summary: Consistently, Nppb-SAP ablated spinal Npr1 and Npr3 neurons and impaired histamine-, but not CQ-evoked, itch. Thus, the findings identify the role of BNP-NPRC signaling in modulation of histamine-evoked itch via NPRC-NMBR cross-talk independent of GRP-GRPR signaling. Our studies reveal distinct modes of action for bombesin-related peptides and NP in itch transmission.
3D Reconstruction of the Neurovascular Unit Reveals Differential Loss of Cholinergic Innervation in the Cortex and Hippocampus of the Adult Mouse Brain. Nizari S, Carare RO, Romero IA, & Hawkes CA. (2019). Front Aging Neurosci, 11 (172). IT-16: mu p75-SAP
Objective: To further characterize the effect of the loss of cholinergic innervation on the NVU (neurovascular unit) in Alzheimer’s Disease.
Summary: Significantly less ChAT staining was detected in the medial septum of saporin-treated mice at 45 days post-surgery. This was accompanied by a significant decrease in cholinergic nerve fiber density in the hippocampus and the cortex. As expected, p75 NTR-negative neurons in the striatum were not affected by mu p75-SAP treatment.
Dose: In this study, the mu-p75-SAP was used to induce death of basal forebrain cholinergic neurons and their fiber projections. mu p75-SAP 0.5 µL (0.596 µg/µL) or 0.9% saline (n = 19) was injected into each ventricle.
Degeneration of ipRGCs in Mouse Models of Huntington’s Disease Disrupts Non-Image-Forming Behaviors Before Motor Impairment. Lin M-S, Liao P-Y, Chen H-M, Chang C-P, Chen S-K, & Chern Y. (2019). J Neurosci, 39 (8):1505. AB-N38: Anti-Melanopsin
Summary: results show that M1 ipRGCs were susceptible to the toxicity caused by mutant Huntingtin. The resultant impairment of M1 ipRGCs contributed to the early degeneration of the ipRGC–SCN pathway and disrupted circadian regulation during HD progression.
Dose: Immunostaining (1:3000)