References

Related publications for ATS products and services
3030 entries

Microglial pannexin-1 channel activation is a spinal determinant of joint pain

Mousseau M, Burma NE, Lee KY, Leduc-Pessah H, Kwok CHT, Reid AR, O’Brien M, Sagalajev B, Stratton JA, Patrick N, Stemkowski PL, Biernaskie J, Zamponi GW, Salo P, McDougall JJ, Prescott SA, Matyas JR, Trang T (2018) Microglial pannexin-1 channel activation is a spinal determinant of joint pain. Sci Adv 4:1-12. doi: 10.1126/sciadv.aas9846

Objective: To identify therapeutic targets for alleviating mechnical allodynia, a sign/symptom of arthritis.

Summary: The pannexin-1 (Panx1) channel is validated as a target; blockade of P2X7 receptors or ablation of spinal microglia prevented and reversed mechanical allodynia.

Usage: Mac-1-SAP and unconjugated Saporin (15 mg per intrathecal injection on days 0, 1, and 2). The specific depletion of spinal lumbar microglia attenuated the development of MIA-induced hypersensitivity indicating that spinal microglia causally contribute to the development of mechanical allodynia. By contrast, intrathecal injection of Control (unconjugated Saporin) did not alter the development of MIA-induced mechanical allodynia.

Related Products: Mac-1-SAP rat (Cat. #IT-33), Saporin (Cat. #PR-01)

Oxytocin attenuates phencyclidine hyperactivity and increases social interaction and nucleus accumben dopamine release in rats.

Kohli S, King MV, Williams S, Edwards A, Ballard TM, Steward LJ, Alberati D, Fone KCF (2019) Oxytocin attenuates phencyclidine hyperactivity and increases social interaction and nucleus accumben dopamine release in rats. Neuropsychopharmacology 44(2):295-305. doi: 10.1038/s41386-018-0171-0

Summary: The authors suggest that further evaluation such as by microinjection with selective antagonists or lesions using the neurotoxin, Oxytocin-SAP, would help delineate the brain region/s and receptor/s involved.

Related Products: Oxytocin-SAP (Cat. #IT-46)

Targeted ablation of cardiac sympathetic neurons attenuates adverse post-infarction remodeling and left ventricle dysfunction.

Xiong L, Liu Y, Zhou M, Wang G, Quan D, Shuai W, Shen C, Kong B, Huang C, Huang H (2018) Targeted ablation of cardiac sympathetic neurons attenuates adverse post-infarction remodeling and left ventricle dysfunction. Exp Physiol 103:1221-1229. doi: 10.1113/EP086928

Objective: To determine whether targeted ablation of cardiac sympathetic neurons (TACSN) could suppress myocardial infarction-induced adverse cardiac remodeling and left ventricle dysfunction.

Summary: TACSN significantly alleviated sympathetic remodeling and neuroendocrine activation, attenuated cardiac hypertrophy and fibrosis, and improved the left ventricular function. Thus, TACSN may have a beneficial effect on adverse post-infarction remodeling and left ventricle dysfunction.

Usage: 20 μl of CTB-SAP (1.2 mg/ml) was mixed with 4 μl of 3% Evans blue dye to make it visible (CTB-SAP is colorless), ensuring localization within the ganglia. The CTB-SAP/Evans blue dye solution was slowly and intermittently injected into the left stellate ganglia using a glass micropipette.

Related Products: CTB-SAP (Cat. #IT-14)

Microtubule-mediated nerve regeneration: Knocking down the microtubule severing protein fidgetin augments nerve regeneration in vitro and in vivo

Matamoros AJ (2018) Microtubule-mediated nerve regeneration: Knocking down the microtubule severing protein fidgetin augments nerve regeneration in vitro and in vivo. Drexel University Thesis.

Objective: To explore the effects of fidgetin knockdown in adult dorsal root ganglia both in vitro and in vivo.

Summary: In vitro: fidgetin knockdown in adult dorsal root ganglia neurons increases a specific domain of microtubule mass responsible for expanding microtubules, increases the length of axons on and off the inhibitory spots, and promotes cellular growth on and across the inhibitory spots. In vivo: fidgetin augments nerve regeneration in vivo, thus highlighting fidgetin as a novel therapeutic target to augment nerve regeneration

Related Products: NGFR (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)

The reduced level of growth factors in an animal model of depression is accompanied by regulated necrosis in the frontal cortex but not in the hippocampus

Kucharczyk M, Kurek A, Pomierny B, Detka J, Papp M, Tota K, Budziszewska B (2018) The reduced level of growth factors in an animal model of depression is accompanied by regulated necrosis in the frontal cortex but not in the hippocampus. Psychoneuroendocrinology 94:121-133. doi: 10.1016/j.psyneuen.2018.05.008 PMID: 29775875

Objective: To investigate if the different types of stress alter neuronal plasticity markers distinctively in the frontal cortex (FCx) and in the hippocampus (Hp).

Summary: The authors concluded that chronic stress during pregnancy can result in serious alterations in the functioning of the FCx of the progeny, facilitating the development of depressive behavior later in life. They also suggest that the altered energy metabolism may redirect pro-NGF/p75NTR/ATF2 signaling in the cortical neurons towards cellular death resembling regulated necrosis, rather than apoptosis.

Usage: Western blot (1:1000)

Related Products: trkA Rabbit Polyclonal (Cat. #AB-N03)

AT2R activation prevents microglia pro-inflammatory activation in a nox-dependent manner: Inhibition of PKC activation and p47(PHOX) phosphorylation by PP2A.

Bhat SA, Sood A, Shukla R, Hanif K (2019) AT2R activation prevents microglia pro-inflammatory activation in a nox-dependent manner: Inhibition of PKC activation and p47(PHOX) phosphorylation by PP2A. Mol Neurobiol 56(4):3005-3023. doi: 10.1007/s12035-018-1272-9 PMID: 30076526

Objective: To investigate the involvement of AT2R in NADPH oxidase (NOX)-mediated microglia activation.

Summary: AT2R, via PP2A-mediated inhibition of PKC, prevents the NOX activation, ROS generation, and subsequent pro-inflammatory activation of microglia.

Usage: Immunoblotting: membranes were incubated with respective primary antibodies AT1R (1:1000), AT2R (1:500). Immunocytochemistry: AT1R (1:100), AT2R (1:100).

Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP), Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)

Conservation of oncofetal antigens on human embryonic stem cells enables discovery of monoclonal antibodies against cancer

Tan HL, Yong C, Tan BZ, Fong WJ, Padmanabhan J, Chin A, Ding V, Lau A, Zheng L, Bi X, Yang Y, Choo A (2018) Conservation of oncofetal antigens on human embryonic stem cells enables discovery of monoclonal antibodies against cancer. Sci Rep 8:11608. doi: 10.1038/s41598-018-30070-z

Objective: To identify and characterize an antibody raised using human embryonic stem cells with potential as a cancer therapeutic.

Summary: Antibody A19 not only binds to undifferentiated hESCs by flow cytometry, it also reacts with ovarian and breast cancer cell lines with low or no binding to normal cells.

Usage: in vitro – Number of viable cells treated showed a decrease in cell number (Hum-ZAP mixed with A19; Streptavidin-ZAP mixed with biotinylated A19). To determine if there were off-target effects, Hum-ZAP and chA19 were incubated with a non-binding cell line OVCAR10; no apparent cytotoxicity was observed. invivo – 5 x 106 SKOV3 cells were implanted s.c. in NUDE mice and Biotinylated A19-Streptavidin-ZAP (ADC), administered ip. The controls were free Saporin and naked A19. By the end of 10 weeks, mice administered with the ADC saw a 60% reduction in tumor size compared to control groups.

Related Products: Hum-ZAP (Cat. #IT-22), Streptavidin-ZAP (Cat. #IT-27), Saporin (Cat. #PR-01)

Serotonin-specific lesions of the dorsal raphe disrupt maternal aggression and caregiving in postpartum rats.

Holschbach MA, Vitale EM, Lonstein JS (2018) Serotonin-specific lesions of the dorsal raphe disrupt maternal aggression and caregiving in postpartum rats. Behav Brain Res 348:53-64. doi: 10.1016/j.bbr.2018.04.008

Objective: To determine the effects of behavioral modifications associated with early motherhood by permanently disrupting serotonin signaling at one of its primary sources, the dorsal raphe (DR).

Summary: Prepartum serotonin-specific lesions of the DRdm impaired maternal aggression. Larger postpartum DR serotonin lesions affected both aggression and caregiving. DR serotonin lesions did not affect postpartum anxiety.

Usage: 1 μL of 0.1M anti-SERT-SAP or control Mouse IgG-SAP was slowly infused into the DR.

Related Products: Anti-SERT-SAP (Cat. #IT-23), Mouse IgG-SAP (Cat. #IT-18)

Effects of cholinergic lesions and cholinesterase inhibitors on aromatase and estrogen receptor expression in different regions of the rat brain

Li J, Rao D, Gibbs RB (2018) Effects of cholinergic lesions and cholinesterase inhibitors on aromatase and estrogen receptor expression in different regions of the rat brain. Neurosci 384:203-213. doi: 10.1016/j.neuroscience.2018.05.033

Objective: To determine if effects of cholinergic inputs on synaptic plasticity and neuronal function are mediated by effects on local estrogen production or ER expression. 

Summary: Selectively destroying cholinergic projections to the hippocampus had little effect on ARO and ER expression in many regions of the rat brain.

Usage: Rats received intraseptal injections of 2.0 ml (0.2 mg/ml) or icv injections of 0.4 mcg.  Lesions resulted in loss of ChAT-positive cells in the septum, and ChAT activity in the hippocampus.  Septal infusions eliminated most of the ChAT-IR cells in MS; ChAT activity in hippocampus also significantly decreased.  ChAT activity in the frontal cortex was not significantly affected.

Related Products: 192-IgG-SAP (Cat. #IT-01)

Retina-specific loss of Ikbkap/Elp1 causes mitochondrial dysfunction that leads to selective retinal ganglion cell degeneration in a mouse model of familial dysautonomia

Ueki Y, Shchepetkina V, Lefcort F (2018) Retina-specific loss of Ikbkap/Elp1 causes mitochondrial dysfunction that leads to selective retinal ganglion cell degeneration in a mouse model of familial dysautonomia. Dis Model Mech 11(7):dmm033746. doi: 10.1242/dmm.033746 PMID: 29929962

Objective: To determine the pathophysiological mechanisms that are triggered by the absence of IKAP (inhibitor of kappa B kinase complex-associated protein) in the retina.

Summary: The loss of IKAP caused progressive degeneration of retinal ganglion cells (RGCs) by 1 month of age. There was no loss of melanopsin+ intrinsically photosensitive RGCs at 18 months. RGCs were the only cell type that degenerated, with the survival of other retinal neurons unaffected.

Usage: Immunohistochemistry (IHC), RGC Counts, and H&E staining – Anti-melanopsin (1:5000).

Related Products: Melanopsin Rabbit Polyclonal (Cat. #AB-N38)

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