References

Related publications for ATS products and services
2938 entries

Two complementary approaches for intracellular delivery of exogenous enzymes

Rust A, Hassan HH, Sedelnikova S, Niranjan D, Hautbergue G, Abbas SA, Partridge L, Rice D, Binz T, Davletov B (2015) Two complementary approaches for intracellular delivery of exogenous enzymes. Sci Rep 5:12444.

Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia.

King T, Ruyle B, Kline D, Heesch C, Hasser E (2015) Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia. Am J Physiol Regul Integr Comp Physiol 309:R721-731. doi: 10.1152/ajpregu.00540.2014

Summary: Catecholaminergic neurons in the brainstem are known to be involved in cardiorespiratory control and to modulate sensory function. Some of the projections from these neurons are to the paraventricular nucleus (PVN), and are involved in cardiorespiratory and neuroendocrine responses to hypoxia. While data have shown the PVN-projecting neurons are activated by hypoxia, their function in this context is not known. In this work the authors bilaterally injected 42 ng of Anti-DBH-SAP (Cat. #IT-03) into the PVN of rats. Mouse IgG-SAP (Cat. #IT-18) was used as control. Respiratory measurements of the lesioned animals indicates that PVN-projecting catecholaminergic neurons are involved in peripheral and central chemoreflex and arterial oxygen levels during exposure to hypoxic stimuli.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

A central role for spinal dorsal horn neurons that express neurokinin-1 receptors in chronic itch.

Akiyama T, Nguyen T, Curtis E, Nishida K, Devireddy J, Delahanty J, Carstens M, Carstens E (2015) A central role for spinal dorsal horn neurons that express neurokinin-1 receptors in chronic itch. Pain 156:1240-1246. doi: 10.1097/j.pain.0000000000000172

Summary: Chronic itch is caused by increased sensitivity of itch-signaling pathways. It can be generated by normally itchy stimuli (hyperknesis) and by normally non-itchy light touch (alloknesis). The authors used an ovalbumin-induced atopic dermatitis model to study chronic itch in mice. The mice received 400-ng intrathecal injections of Bombesin-SAP (Cat. #IT-40), SSP-SAP (Cat. #IT-11), or the control Blank-SAP (Cat. #IT-21). While Bombesin-SAP significantly attenuated hyperknesis, it had no effect on spontaneous scratching or alloknesis. SSP-SAP reduced all behavioral signs of chronic itch.

Related Products: Bombesin-SAP (Cat. #IT-40), SSP-SAP (Cat. #IT-11), Blank-SAP (Cat. #IT-21)

Featured Article: SP-SAP human clinical trial for cancer pain – an anesthesiologist’s point of view

Noe C, McDermott E (2015) Featured Article: SP-SAP human clinical trial for cancer pain – an anesthesiologist’s point of view. Targeting Trends 16(3)

Related Products: SP-SAP (Cat. #IT-07)

Read the featured article in Targeting Trends.

Selective C1 lesioning slightly decreases angiotensin II type I receptor expression in the rat rostral ventrolateral medulla (RVLM).

Bourassa E, Stedenfeld K, Sved A, Speth R (2015) Selective C1 lesioning slightly decreases angiotensin II type I receptor expression in the rat rostral ventrolateral medulla (RVLM). Neurochem Res 40:2113-2120. doi: 10.1007/s11064-015-1649-3

Summary: Exogenous angiotensin II administered to the RVLM produces a significant pressor response that can be countered by angiotensin II type I receptor antagonists. In this work the authors examined the relative contribution of C1 and non-C1 neurons in the RVLM to this angiotensin II response. Rats received 10 or 15 ng of Anti-DBH-SAP (Cat. #IT-03) as unilateral injections into the RVLM. Mouse IgG-SAP (Cat. #IT-18) was used as control. The data indicate that the majority of angiotensin II type 1 receptors are expressed on non-C1 neurons or glia.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

Monoclonal antibodies targeting LecLex-related glycans with potent antitumor activity.

Chua J, Vankemmelbeke M, McIntosh R, Clarke P, Moss R, Parsons T, Spendlove I, Zaitoun A, Madhusudan S, Durrant L (2015) Monoclonal antibodies targeting LecLex-related glycans with potent antitumor activity. Clin Cancer Res 21:2963-2974. doi: 10.1158/1078-0432.CCR-14-3030

Summary: In this work the authors characterized two monoclonal antibodies that target glycans containing Lewis carbohydrate antigens. One of the methods used was to combine varying concentrations of the antibodies with 50 ng mouse Fab-ZAP (Cat. #IT-48) and apply the conjugates to cells for 72 hours. The antibodies were demonstrated to have efficient internalization, supported by potent in vivo anti-tumor activity.

Related Products: Fab-ZAP mouse (Cat. #IT-48)

proBDNF and p75NTR control excitability and persistent firing of cortical pyramidal neurons.

Gibon J, Buckley S, Unsain N, Kaartinen V, Séguéla P, Barker P (2015) proBDNF and p75NTR control excitability and persistent firing of cortical pyramidal neurons. J Neurosci 35:9741-9753. doi: 10.1523/JNEUROSCI.4655-14.2015 PMID: 26134656

Summary: Principal neurons in the entorhinal cortex (EC) display persistent firing (PF) during working-memory tasks. Much of the communication between the hippocampus and the neocortex passes through the EC, and the EC also receives some cholinergic input from the medial septum and diagonal band of Broca. In this work the authors investigated the role of pro-brain-derived neurotrophic factor (proBDNF) and the p75 receptor in excitability and PF in the EC. The authors propose the proBDNF/p75 system as a regulator for pyramidal neuron excitability and PF in the EC, preventing runaway activity. Some of the western blot and current-clamp data was generated using Anti-p75 (Cat. #AB-N01; no concentration information provided).

Related Products: NGFr (mu p75) Rabbit Polyclonal (Cat. #AB-N01)

Retrograde transport is not required for cytosolic translocation of the B-subunit of Shiga toxin.

Garcia-Castillo M, Tran T, Bobard A, Renard H, Rathjen S, Dransart E, Stechmann B, Lamaze C, Lord M, Cintrat J, Enninga J, Tartour E, Johannes L (2015) Retrograde transport is not required for cytosolic translocation of the B-subunit of Shiga toxin. J Cell Sci 128:2373-2387. doi: 10.1242/jcs.169383

Summary: Bacterial and plant toxins rely on various trafficking pathways to reach intracellular targets. Shiga and Shiga-like toxins have been found to be moved via vesicular transport through several subcellular structures on the way to the cytosol. Shiga toxin (STx) is the cause of hemolytic uremic syndrome, for which there is no effective treatment. In order to better understand the mechanisms of STx membrane translocation the authors used a custom conjugate of the receptor-binding B-subunit of STx (STxB) and saporin (Custom conjugation provided by Advanced Targeting Systems). In vitro assays demonstrated that STxB-SAP did not use retrograde transport to the Golgi complex in order to reach the cytosol. This information has relevance to antigen cross-presentation of antigen-presenting cells.

Related Products: Custom Conjugates

Different immune cells mediate mechanical pain hypersensitivity in male and female mice.

Sorge R, Mapplebeck J, Rosen S, Beggs S, Taves S, Alexander J, Martin L, Austin J, Sotocinal S, Chen D, Yang M, Shi X, Huang H, Pillon N, Bilan P, Tu Y, Klip A, Ji R, Zhang J, Salter M, Mogil J (2015) Different immune cells mediate mechanical pain hypersensitivity in male and female mice. Nat Neurosci 18:1081-1083. doi: 10.1038/nn.4053

Summary: A large and rapidly increasing body of evidence indicates that microglia-to-neuron signaling is essential for chronic pain hypersensitivity. Using multiple approaches, the authors found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypersensitivity using adaptive immune cells, likely T lymphocytes. This sexual dimorphism suggests that male mice cannot be used as proxies for females in pain research. Mac-1-SAP mouse/human toxin (Cat. #IT-06, 15 μg in 8.8 μl) and Saporin control (Cat. #PR-01, 8.8 μg in 8.8 μl) were administered via i.t. injection. The topic of immune system involvement in chronic pain pathophysiology is one of the most active in the pain field; that this sex difference has not been observed until now is very surprising indeed. An important implication of the current findings is that distinct strategies targeting neuroimmune signaling might be required for the treatment of chronic pain in men versus women.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06), Saporin (Cat. #PR-01)

Inflammatory macrophages promotes development of diabetic encephalopathy.

Wang B, Miao Y, Zhao Z, Zhong Y (2015) Inflammatory macrophages promotes development of diabetic encephalopathy. Cell Physiol Biochem 36:1142-1150. doi: 10.1159/000430285

Summary: Diabetes can cause neuroinflammation leading to dementia. Diabetes was induced in mice by injection of streptozotocin (STZ). In order to investigate the role of inflammatory macrophages in the development of diabetic encephalopathy, the authors used twice weekly 20-μg IP injections of Mac-1-SAP (Cat. #IT-06). Mice receiving Mac-1-SAP had significantly reduced numbers of inflammatory macrophages in the brain, and also reduced responses to STZ injection.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)

Shopping Cart
Scroll to Top