Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High performance liquid chromatography (HPLC) was employed as a means of analyzing estrogen receptor (ER)-antibody recognition. This technique takes advantage of the fact that the majority of gamma-globulin-antigen complexes do not interact with the anion-exchange resins selected. A variety of monoclonal (MAb) and polyclonal antibodies (PAb) raised against ER and ER-associated proteins were assessed for their chromatographic behaviour after association with charged ER, based upon properties of size, shape, and surface charge. ER exhibits polymorphism, several isoforms being present in target cells. The monoclonal antibody H222Sp gamma demonstrated discrete specificity for the 150 mM ER isoform (normally eluting at 150 mM phosphate) from the high-performance ion-exchange chromatography column which was eluted unretained when complexed with antibody. However, the monoclonal reagent D547Sp gamma interacted directly with anion-exchange columns (SynChropak AX-1000 and Altex DEAE-5PW), complicating a clear evaluation of ER-MAb association. Only 50-60% of the 150 mM ER isoform was eluted at a lower salt concentration. Few conclusions could be drawn with respect to MAb interaction with the 50-60 mM ER isoform (normally eluting at 50-60 mM phosphate) since the antibody-receptor complex was also eluted at the same phosphate concentration. In addition, polyclonal and monoclonal antibodies to the ER and ER-associated proteins were assessed by HPLC. At present, heat shock proteins and protein kinase activity have been shown by other techniques to be associated with the ER. Size-exclusion resins, such as TSK 3000 SW, were employed in a fast method of determining ER isoform-antibody recognition. Thus, HPLC may be used to analyze soluble antibody-antigen interactions rapidly, with high recovery of biological activity.
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PMID:Assessment of estrogen receptor-monoclonal antibody interaction by high-performance liquid chromatography. 244 25

The objective of this study was to investigate the chemopreventive potentials of glycine- and proline-rich glycoprotein (SNL glycoprotein, 150-kDa) isolated from Solanum nigrum Linne on formation of colonic aberrant crypt foci (ACF) induced by 1,2-dimethylhydrazine (DMH, 20 mg/kg) in A/J mice. Administration of SNL glycoprotein inhibited phosphorylation of extracellular signal-regulated kinase (ERK), expression of colonic proliferating cell nuclear antigen (PCNA), and frequency of colonic ACF in DMH-stimulated mice colon carcinogenesis. In addition, SNL glycoprotein increased expression of cyclin-dependent kinase inhibitors (p21(WAF/Cip1) and p27(Kip1)), whereas reduced expression of precursor form of apoptosis-related proteins [pro-caspase-3 and pro-poly(ADP-ribose)polymerase (PARP)] in the mice. Interestingly, the results in this study revealed that SNL glycoprotein has suppressive effects on activity of nuclear factor-kappa B (NF-kappaB), whereas it has stimulatory effect on the expression of p53, accompanying inhibitory effects on expression of NF-kappaBp50, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin (IL)-6, and tumor necrosis factor (TNF)-alpha in DMH-stimulated ACF formation. Also, SNL glycoprotein has inhibitory effects on the formation of thiobarbituric acid reactive substances (TBARS), on the production of inducible nitric oxide (NO), and on the release of lactate dehydrogenase (LDH) in the mice plasma. Collectively, our findings in this study suggest that SNL glycoprotein has chemopreventive activity via modulation of cell proliferation and apoptosis in DMH-treated A/J mice.
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PMID:Glycine- and proline-rich glycoprotein regulates the balance between cell proliferation and apoptosis for ACF formation in 1,2-dimethylhydrazine-treated A/J mice. 1918 65

A differential role of endothelin-1 (ET-1) in pain processing has recently been suggested. However, the function of central ET-1 in neuropathic pain (NP) has not been fully elucidated to date. We report here the action of endogenous central ET-1 in sciatic nerve ligation-induced NP (SNL-NP) in a transgenic animal model that over-expresses ET-1 in the astrocytes (GET-1 mice). We hypothesized that the over-expression of astrocytic ET-1 would exert anti-allodynic and anti-hyperalgesic effects in NP, as demonstrated by mechanical threshold and plantar withdrawal latency using the von Frey filament and heat stimuli. In our animal model, GET-1 mice showed an increase in the withdrawal threshold and latency in response to the mechanical and thermal stimuli, respectively, in pain behavior tests after SNL. ET-1 and endothelin type A receptor (ETA-R) levels were increased significantly in L4-L6 segments of the spinal cord (ipsilateral to SNL) of GET-1 mice at 7 and 21days after surgery. Moreover, intrathecal administration of a specific ETA-R antagonist, BQ-123, attenuated the anti-allodynic and anti-hyperalgesic phenotype in GET-1 mice. The effects of BQ-123 on the mRNA expression of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and protein kinase B/serine protein kinase (Akt(s)) were assessed in the ipsilateral L4-L6 segments harvested 30min after BQ-123 administration on day 7 after surgery. Phosphorylation of ERK1/2 and Akt(s) in the ipsilateral spinal cord of GET-1 mice was reduced following SNL, whereas no reduction was observed after intrathecal injection of BQ-123. In conclusion, our results showed that the xover-expression of astrocytic ET-1 reduced SNL-induced allodynia and hyperalgesia by inhibiting the activation of ERK1/2 and Akt(s) via the ETA-R-mediated pathway.
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PMID:Over-expression of astrocytic ET-1 attenuates neuropathic pain by inhibition of ERK1/2 and Akt(s) via activation of ETA receptor. 2459 54