CD70 (TNFSF7) is expressed at high prevalence in renal cell carcinomas and is rapidly internalised on antibody binding.
Adam PJ, Terrett JA, Steers G, Stockwin L, Loader JA, Fletcher GC, Lu LS, Leach BI, Mason S, Stamps AC, Boyd RS, Pezzella F, Gatter KC, Harris AL.
Br J Cancer 95(3):298-306, 2006.
Renal cell carcinoma (RCC) is usually resistant to chemotherapy. The authors found a potential target for immunotherapy. An antibody against CD70 was combined with Hum-ZAP (Cat. #IT-22). The complex was then added to an RCC-derived cell-line in vitro, demonstrating significant killing at several different concentrations.
Adenosine and sleep homeostasis in the Basal forebrain.
Blanco-Centurion C, Xu M, Murillo-Rodriguez E, Gerashchenko D, Shiromani AM, Salin-Pascual RJ, Hof PR, Shiromani PJ.
J Neurosci 26(31):8092-8100, 2006.
The authors investigated whether basal forebrain cholinergic neurons are involved in adenosine regulation of sleep. 6 µg of 192-IgG-SAP (Cat. #IT-01) was administered to the lateral ventricle of rats. In treated animals, adenosine levels did not increase with prolonged waking.
Secondary hyperalgesia in the monoarthritic rat is mediated by GABAB and NK1 receptors of spinal dorsal horn neurons: a behavior and c-fos study.
Castro AR, Pinto M, Lima D, Tavares I.
Neuroscience 141(4):2087-2095, 2006.
Hallmarks of secondary hyperalgesia in a rat model of monoarthritic pain are: decreased activation of GABA(B) neurons, and increased activation of NK-1r neurons. Using 10-µl injections of 1-µM SP-SAP (Cat. #IT-07) into T(13)-L(1) the authors looked at the role of each receptor. Results indicate that both GABA(B) and NK-1r are involved in secondary hyperalgesia.
High-affinity ligand probes of CD22 overcome the threshold set by cis ligands to allow for binding, endocytosis, and killing of B cells.
Collins BE, Blixt O, Han S, Duong B, Li H, Nathan JK, Bovin N, Paulson JC.
J Immunol 177(5):2994-3003, 2006.
CD22, a member of the siglec subgroup of the Ig superfamily, is a potential target for immunotherapy of B cell lymphomas. The authors demonstrate that a biotinylated probe specific for CD22 combined with streptavidin-ZAP (Cat. #IT-27), can eliminate several different lymphoma cell lines.
Immunolesions of glucoresponsive projections to the arcuate nucleus alter glucoprivic-induced alterations in food intake, luteinizing hormone secretion, and GALP mRNA, but not sex behavior in adult male rats.
Neuroendocrinology 83(2):97-105, 2006.
In this work the author looked at the role hypothalamic glucose may play in reproductive function. 42 ng of anti-DBH-SAP (Cat. #IT-03) was injected dorsal of the arcuate nucleus of rats, which were then given glucoprivic challenges. The data demonstrate the involvement of A1/C1 efferents to the ventromedial hypothalamus in glucostatic regulation of various processes.
The nuclear DNA repair protein Ku70/80 is a tumor-associated antigen displaying rapid receptor mediated endocytosis.
Fransson J, Borrebaeck CA.
Int J Cancer 119(10):2492-2496, 2006.
In this study, the authors show that Ku70/80 is internalized into pancreatic carcinoma cells upon binding of the antibody INCA-X. INCA-X was combined with Mab-ZAP (Cat. #IT-04) and applied to several pancreatic carcinoma cell lines in vitro. Cell death in some of the treated lines demonstrates the potential of Ku70/80 as a therapeutic target.
Lack of neurogenesis in the adult rat cerebellum after Purkinje cell degeneration and growth factor infusion.
Grimaldi P, Rossi F.
Eur J Neurosci 23(10):2657-2668, 2006.
Although neurogenesis occurs in very specific areas of the mammalian brain, neural progenitors can be found in many central nervous system sites. Here the authors examined neurogenesis in the rat cerebellum. 2.2 µg of 192-IgG-SAP (Cat. #IT-01) was injected into each lateral ventricle, and some animals were given exogenous EGF, bFGF, or FGF8. In this model, the local environment was not sufficient to direct neuronal differentiation, even with the addition of growth factors.
Ameliorating effect of saporin-conjugated anti-CD11b monoclonal antibody in a murine T-cell-mediated chronic colitis.
Kanai T, Uraushihara K, Totsuka T, Nemoto Y, Fujii R, Kawamura T, Makita S, Sawada D, Yagita H, Okumura K, Watanabe M.
J Gastroenterol Hepatol 21(7):1136-1142, 2006.
Using SCID mice, the authors evaluated the effects of Mac-1-SAP (Cat. #IT-06) on the development of chronic colitis. After transfer of T cells to the mice, 12.5 µg of Mac-1-SAP was injected into the intraperitoneal space. The reduction in CD4(+) T-cell infiltration of the colon, and suppression of IFNγ and TNFα production indicate that macrophages play a significant role in the pathogenesis of Crohn’s disease.
Neurokinin-1 receptor-expressing neurons in the ventral medulla are essential for normal central and peripheral chemoreception in the conscious rat.
Nattie E, Li A.
J Appl Physiol 101(6):1596-1606, 2006.
The authors ask if neurokinin-1 receptor (NK-1r)-positive cells scattered throughout the ventral medulla are involved in central and peripheral chemoreception. Rats received 250-280 ng of SSP-SAP (Cat. #IT-11) into the cisterna magna; mouse IgG-SAP (Cat. #IT-18) was used as a control. The results indicate that NK-1r neurons in the ventral medulla are involved in both central and peripheral chemoreception, during both waking and sleep states.
Purkinje cell loss by OX7-saporin impairs acquisition and extinction of eyeblink conditioning.
Nolan BC, Freeman JH.
Learn Mem 13(3):359-365, 2006.
This work examines the effect of a global depletion of Purkinje cells in the cerebellar cortex on delay eyeblink conditioning in rats. 15 µg of OX7-SAP (Cat. #IT-02) was infused into the left lateral ventricle 2 weeks prior to training. Purkinje cell loss in the anterior lobe and lobule HVI correlated with impaired acquisition and extinction of delay eyeblink conditioning.
Cortical choline transporter function measured in vivo using choline-sensitive microelectrodes: clearance of endogenous and exogenous choline and effects of removal of cholinergic terminals.
Parikh V, Sarter M.
J Neurochem 97(2):488-503, 2006.
The authors investigated the role of high-affinity choline transporters (CHT) in the clearance of exogenous choline, as well as choline from newly released acetylcholine. 0.085 µg of 192-IgG-SAP (Cat. #IT-01) was injected into each hemisphere of the basal forebrain of rats (mouse IgG-SAP, Cat. #IT-18, was used as a control). The results demonstrate that no matter the source, increases in choline concentrations are cleared by CHT’s.
Hindbrain catecholamine neurons control multiple glucoregulatory responses.
Ritter S, Dinh TT, Li AJ.
Physiol Behav 89(4):490-500, 2006.
The authors focus on mechanisms eliciting glucoregulatory responses; in particular the catecholaminergic neurons in the hindbrain. Rats received injections of anti-DBH-SAP (Cat. #IT-03) into epinephrine (E) and norepinephrine (NE) terminal areas of hypothalamus and spinal cord. The data suggest that E/NE neurons coordinate various components of the behavioral response to glucoprivation.
Local and descending circuits regulate long-term potentiation and zif268 expression in spinal neurons.
Rygh LJ, Suzuki R, Rahman W, Wong Y, Vonsy JL, Sandhu H, Webber M, Hunt S, Dickenson AH.
Eur J Neurosci 24(3):761-772, 2006.
Long-term potentiation (LTP) has been shown to occur in sensory areas of the spinal cord and may be one of the mechanisms by which acute pain is transformed into chronic pain. 10 µl of 1µM SP-SAP (Cat. #IT-07) or saporin (Cat. #PR-01) were injected into the subarachnoid space (L4-L5) of rats. The authors demonstrate that dorsal horn neuron generation of LTP may transform acute pain into chronic pain.
Descending facilitation from the rostral ventromedial medulla maintains nerve injury-induced central sensitization.
Vera-Portocarrero LP, Zhang ET, Ossipov MH, Xie JY, King T, Lai J, Porreca F.
Neuroscience 140(4):1311-1320, 2006.
Rats were treated with 1.5 pmol of dermorphin-SAP (Cat. #IT-12) or saporin (Cat. #PR-01) into each side of the rostral ventromedial medulla, followed by spinal nerve ligation. The data indicate that mu opioid-expressing neurons are necessary to maintain nerve injury-induced central sensitization.