References

Related publications for ATS products and services
2914 entries

Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats

Dobryakova YV, Volobueva MN, Manolova AO, Medvedeva TM, Kvichansky AA, Gulyaeva NV, Markevich VA, Stepanichev MY, Bolshakov AP (2019) Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats. Front Neurosci 13:146. doi: 10.3389/fnins.2019.00146

Objective: To study the histopathology of the hippocampus and the responses of microglia and astrocytes using immunohistochemistry and neuroglial gene expression.

Summary: Cholinergic degeneration in the medial septal area induced by intracerebroventricular administration of 192IgG-saporin results in an increase in the number of microglial cells and neuron degeneration in the dorsal hippocampus.

Usage: 192-IgG-SAP was injected bilaterally into both ventricles (i.c.v.) at a dose of 4 μg/site.

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

Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target.

Bahari Z, Meftahi GH (2019) Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target. Br J Pharmacol 176(14):2366-2381. doi: 10.1111/bph.14580

Objective: To provide an an overview of the cellular mechanisms through which brainstem adrenergic descending inhibitory processing can alter spinal pain transmission to the higher centres, and how these pathways change in neuropathic pain conditions focusing on the role of spinal α2‐adrenoceptors in the spinal dorsal horn.

Summary: The α2‐adrenoceptor agonist may be useful to treat neuropathic pain.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Noradrenergic terminals are the primary source of α2-adrenoceptor mediated dopamine release in the medial prefrontal cortex.

Devoto P, Flore G, Saba P, Scheggi S, Mulas G, Gambarana C, Spiga S, Gessa GL (2019) Noradrenergic terminals are the primary source of α2-adrenoceptor mediated dopamine release in the medial prefrontal cortex. Prog Neuropsychopharmacol Biol Psychiatry 90:97-103. doi: 10.1016/j.pnpbp.2018.11.015

Objective: To clarify the relative contribution of dopamine (DA) release from noradrenergic and dopaminergic terminals to DA output induced by blockade of α2-adrenoreceptors and the norepinephrine transporter.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Palladium based nanoparticles for the treatment of advanced melanoma.

Elsey J, Bubley JA, Zhu L, Rao S, Sasaki M, Pollack BP, Yang L, Arbiser JL (2019) Palladium based nanoparticles for the treatment of advanced melanoma. Sci Rep 9:3255. doi: 10.1038/s41598-019-40258-6 PMID: 30824801

Usage: immunohistochemistry (1:300)

Related Products: Fibroblast Growth Factor Rabbit Polyclonal, mammalian (Cat. #AB-07)

Combining naproxen and a dual amylin and calcitonin receptor agonist improves pain and structural outcomes in the collagen-induced arthritis rat model.

Katri A, Dąbrowska A, Löfvall H, Ding M, Karsdal MA, Andreassen KV, Thudium CS, Henriksen K (2019) Combining naproxen and a dual amylin and calcitonin receptor agonist improves pain and structural outcomes in the collagen-induced arthritis rat model. Arthritis Res Ther 21(1):68. doi: 10.1186/s13075-019-1819-9 PMID: 30795801

Objective: To investigate if combining a standard of care NSAID (naproxen) with a Key Bioscience peptides (KBP) resulted in improvement in pain scores, as well as disease activity and structural damage in a rat model of rheumatoid arthritis (RA).

Summary: Combination therapy had improved efficacy over naproxen monotherapy; combination therapy resulted in improved health scores, and reduced mechanical and cold allodynia assessment. Furthermore, protection of articular cartilage structure and preservation of bone structure and bone volume were also observed.

Usage: histology (1:4000)

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

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) Degeneration of ipRGCs in mouse models of huntington’s disease disrupts non-image-forming behaviors before motor impairment. J Neurosci 39(8):1505. doi: 10.1523/JNEUROSCI.0571-18.2018 PMID: 30587542

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.

Usage: Immunostaining (1:3000)

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

Sacituzumab for the treatment of triple-negative breast cancer: the poster child of future therapy?

Zangardi ML, Spring LM, Nagayama A, Bardia A (2019) Sacituzumab for the treatment of triple-negative breast cancer: the poster child of future therapy?. Expert Opin Investig Drugs 28(2):107-112. doi: 10.1080/13543784.2019.1555239 PMID: 30507322

Summary: This publication explores the potential of sacituzumab as a treatment for triple-negative breast cancer, highlighting its promising role as a leading candidate for future therapeutic approaches. The study suggests that sacituzumab may represent a breakthrough in the management of this aggressive breast cancer subtype, raising hopes for improved outcomes in patients.

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.

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 (2019) 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. J Med Chem 62(3):1203-1217. doi: 10.1021/acs.jmedchem.8b01280

Objective: To discover and develop a therapeutic for human sleep disorders.

Summary: Histamine H3 Receptor Inverse Agonist demonstrated high receptor occupancy and marked wake promoting effects with decreased REM sleep in Orexin-B-SAP lesioned rats. This study supports its potential therapeutic utility in treating human sleep disorders.

Usage: Injections (490 ng/0.8 μl) were made bilaterally to the lateral hypothalamus.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Selective hematopoietic stem cell ablation using CD117-antibody-drug-conjugates enables safe and effective transplantation with immunity preservation.

Czechowicz A, Palchaudhuri R, Scheck A, Hu Y, Hoggatt J, Saez B, Pang WW, Mansour MK, Tate TA, Chan YY, Walck E, Wernig G, Shizuru JA, Winau F, Scadden DT, Rossi DJ (2019) Selective hematopoietic stem cell ablation using CD117-antibody-drug-conjugates enables safe and effective transplantation with immunity preservation. Nat Commun 10:617. doi: 10.1038/s41467-018-08201-x

Objective: To investigate a safe and effective method for hematopoietic stem cell transplantation.

Summary: CD117-ADC selectively targets hematopoietic stem cells yet does not cause clinically significant side-effects.

Usage: The CD117-ADC was prepared by combining biotinylated anti-CD117 (clone 2B8) with Streptavidin–ZAP. A dose of 1.5 mg/kg of CD117-ADC (~12 µg Streptavidin-ZAP) optimally resulted in depletion of >99% of immunophenotypic and functional HSCs.

Related Products: Streptavidin-ZAP (Cat. #IT-27), Anti-CD117-SAP (Cat. #IT-83)

Hematopoietic chimerism and donor-specific skin allograft tolerance after non-genotoxic CD117 antibody-drug-conjugate conditioning in MHC-mismatched allotransplantation.

Li Z, Czechowicz A, Scheck A, Rossi DJ, Murphy PM (2019) Hematopoietic chimerism and donor-specific skin allograft tolerance after non-genotoxic CD117 antibody-drug-conjugate conditioning in MHC-mismatched allotransplantation. Nat Commun 10:616. doi: 10.1038/s41467-018-08202-w

Objective: To develop a conditioning protocol for fully MHC-mismatched bone marrow allotransplantation in mice involving transient immunosuppression and selective depletion of recipient hematopoietic stem cells.

Summary: CD117-ADC conditioning promotes skin allograft tolerance.

Usage: Biotinylated monoclonal antibodies directed against mouse CD117 were coupled to Streptavidin-ZAP. Each mouse was injected with 1.5 mg/kg of ADC in a total volume of 300 mcl PBS.

Related Products: Streptavidin-ZAP (Cat. #IT-27)

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