Biomedical subjects

Y S Song

Publications and source records attributed to Y S Song.

At least 37 records · Page 2Linked to original sources

PubMed2001

Antiplatelet mechanism of 2-chloro-3-(4-hexylphenyl)-amino-1,4-naphthoquinone (NQ304), an antithrombotic agent.

The effects of 2-chloro-3-(4-hexylphenyl)-amino-1,4-naphthoquinone (NQ304), an antithrombotic agent, on aggregation, binding of fibrinogen to glycoprotein IIb/IIIa and intracellular signals were investigated using human platelets. NQ304 inhibited thrombin-, arachidonic acid- and thapsigargin-induced aggregation of washed human platelets with the IC50 values of 22.2+/-0.7, 6.5+/-0.2, and 7.6+/-0.1 microM, respectively. NQ304 significantly inhibited fluorescein isothiocyanate-conjugated fibrinogen binding to human platelet surface glycoprotein IIb/IIIa receptor by 75%, but failed to inhibit the fibrinogen binding to purified glycoprotein IIb/IIIa receptor. This result suggests that NQ304 inhibit platelet aggregation by suppression of an intracellular pathway that involves exposure of the glycoprotein IIb/IIIa receptor, rather than by direct inhibition of fibrinogen-glycoprotein IIb/IIIa binding. NQ304 significantly inhibited thrombin-induced increase in intracellular Ca2+ mobilization at the dose of 30 microM and ATP secretion in a dose-dependent manner. It also inhibited thrombin- and arachidonic acid-induced thromboxane A2 formation in human platelet dose-dependently. In conclusion, the antiplatelet mechanism of NQ304 may be due to the reduction of the thromboxane A2 formation, inhibition of adenosine triphosphate release and intracellular calcium mobilization.

Adenosine Triphosphate↗

PubMed2001

Is there a role of radial rigidity in the evaluation of erectile dysfunction?

RigiScan has been the most widely utilized device for measuring erectile rigidity. However, the use of the RigiScan in the evaluation of erectile dysfunction has questionable because the RigiScan device does not directly determine axial rigidity. The aim of this study is to clarify that radial rigidity measured by RigiScan reflects the intracorporeal pressure and erectile capability efficiently. From January 1998 to May 1999, a total of 23 patients with erectile dysfunction were involved in the study. They were evaluated by RigiScan and duplex ultrasonography after intracorporeal injection of prostaglandin E1. We investigated the relationship between radial rigidity and the resistance index. The results of radial rigidity were also compared with that of the degree of erection. For the entire group, significant correlations were found between radial rigidity and the resistance index (r=0.680, P<0.001 for tip rigidity; r=0.703, P<0.001 for base rigidity). In addition, for 12 patients whose tip rigidity exceeded 60% and for 10 whose base rigidity exceeded 60%, the correlations between radial rigidity and the resistance index remained (r=0.659, P=0.020 for tip rigidity; r=0.759, P=0.011 for base rigidity). Based on the response determined by patients, radial rigidity represented the degree of erection efficiently. Our findings suggest that RigiScan is a useful diagnostic tool. Radial rigidity represents the intracorporeal pressure efficiently and has an acceptable role in the evaluation of erectile dysfunction.

Adult↗

PubMed2001

Polymorphism of TP53 codon 72 and the risk of cervical cancer among Korean women.

OBJECTIVE: It has recently been suggested that white women who are homozygous for the allele of the gene for wild-type p53 protein (TP53) that encodes arginine at position 72 are more susceptible to human papillomavirus-associated cervical carcinoma than are women who are heterozygous for this polymorphism and women who are homozygous for the allele that encodes proline at that position. This study was undertaken to analyze whether the TP53 codon 72 single-nucleotide polymorphism might be correlated with the risk of cervical cancer among Korean women. STUDY DESIGN: Peripheral blood samples from patients with invasive cervical carcinoma yielding a positive result for human papillomavirus 16 (n = 100), patients with cervical intraepithelial neoplasia grade III (n = 134), and healthy control subjects (n = 100) were examined. The presence and genotype of human papillomavirus in cancerous cervical tissues were determined by E6, E7-based nested polymerase chain reaction. Germline genomic deoxyribonucleic acid was extracted from peripheral blood leukocytes and examined by polymerase chain reaction amplification of the specific allele assay as described by Storey et al. Deoxyribonucleic acid samples from patients whose TP53 sequences had been determined by direct sequencing were used as positive control preparations. RESULTS: The respective proportions of individuals who are homozygous for the arginine allele, homozygous for the proline allele, and heterozygous for the 2 alleles were 40%, 12%, and 48% among women with invasive cervical carcinoma, 52%, 9%, and 39% among women with cervical intraepithelial neoplasia grade III, and 52%, 11%, and 37% among the control group. No significant differences in the frequency of codon 72 alleles were found among the 3 groups (chi(2) = 4.414; P =.353; degrees of freedom = 4). CONCLUSION: This finding suggests that the risk of cervical cancer may not be increased for Korean women with the allele of TP53 encoding arginine at codon 72.

Antibodies, Viral↗

PubMed2001

Phosphatidylinositol 3-kinase regulates proliferation of RAW 264.7 macrophages.

Phosphatidylinositol 3-kinase (P13-kinase) is an enzyme that acts as a direct biochemical link between a novel phosphatidylinositol pathway and a number of proteins containing intrinsic or associated kinase activities. Here we demonstrate that wortmannin, P13-kinase inhibitor, decreases the proliferation of RAW 264.7 macrophages and that another structurally unrelated inhibitor of P13-kinase, LY294002. also inhibits the proliferation. These results indicate a possible involvement of P13-kinase in RAW 264.7 macrophages growth regulation. Wortmannin stimulation of RAW 264.7 macrophages is followed by sustained expression of the mRNA of c-fos and a transient expression of the mRNA of c-jun. We also show that the wortmannin and LY294002 induce a cell cycle arrest in asynchronously growing cells leading to an inhibition of cell proliferation after 12 h of treatment. In addition, wortmannin or LY294002 inhibited the phorbol 12-myristate 13-acetate-induced macrophages proliferation potently. These results suggest that P13-kinase plays an important role in growth regulation of RAW 264.7 macrophages and that protein kinase C is a down stream effector of P13-kinase.

Androstadienes↗

PubMed2000

Determination of amphetamine and methamphetamine in serum via headspace derivatization solid-phase microextraction-gas chromatography-mass spectrometry.

This study evaluates solid-phase microextraction (SPME) coupled with gas chromatography-mass spectrometry (GC-MS) to determine trace levels of amphetamine and methamphetamine in serum. Headspace post-derivatization in a laboratory-made design with heptafluorobutyric anhydride vapor following SPME was compared with that without derivatization SPME. The SPME experimental procedures to extract amphetamine and methamphetamine in serum were optimized with a relatively non-polar poly(dimethylsiloxane) coated fiber at pH 9.5, extraction time for 40 min and desorption at 260 degrees C for 2 min. Experimental results indicate that the concentration of the serum matrix diluted to a quarter of original (1:3) ratio by using one volume of buffer solution of boric acid mixed with sodium hydroxide and two volumes of water improves the extraction efficiency. Headspace derivatization following SPME was performed by using 6 microl 20% (v/v) heptafluorobutyric anhydride ethyl acetate solution at an oil bath temperature of 270 degrees C for 10 s. The precision was below 7% for analysis for without derivatization and below 17% for headspace derivatization. Detection limits were obtained at the ng/l level, one order better obtained in headspace derivatization than those achieved without derivatization. The feasibility of applying the methods to determine amphetamine and methamphetamine in real samples was examined by analyzing serum samples from methamphetamine abused suspects. Concentrations of the amphetamine and methamphetamine ranged from 6.0 microg/l (amphetamine) to 77 microg/l (methamphetamine) in serum.

Amphetamines↗

PubMed2000

The role of the hinge region of the luteinizing hormone receptor in hormone interaction and signal generation.

Luteinizing hormone receptor, a G protein-coupled receptor, consists of two halves, the N-terminal extracellular hormone binding domain (exodomain) and the C-terminal membrane-associated, signal-generating domain (endodomain). The exodomain has seven to nine Leu-rich repeats, which are generally thought to form a 1/3 donut-like structure and interact with human choriogonadotropin (hCG). The resulting hCG-exodomain complex adjusts the structure and its association with the endodomain, which results in signal generation in the endodomain. It is unclear whether the rigid 1/3 donut structure could provide the agility and versatility of this dynamic action. In addition, there is no clue as to where the endodomain contact point (the signal modulator) in the exodomain is. To address these issues, the exodomain was examined by Ala scan and multiple substitutions, while receptor peptides were used for photoaffinity labeling and affinity cross-linking. Our results show that the C-flanking sequence (hinge region), Thr(250)-Gln(268), of the Leu-rich repeats (LRRs) specifically interacts with hCG, preferentially hCGalpha. This interaction is inhibited by exoloop 2 of the endodomain but not by exoloops 1 and 3, suggesting an intimate relationship between Thr(250)-Gln(268), exoloop 2, and hCG. Taken together, our observations in this article suggest a new paradigm that the LRRs contact the front of hCG, while both flanking regions of the LRRs interact with the sides of hCG. This would trap hCG in the 1/3 donut structure of the LRRs and enhance the binding affinity. In addition, mutations of conserved Ser(255) in the sequence can constitutively activate the receptor. This provides a clue for the signal modulator in the exodomain. In contrast, a phenyl or phenolic group is necessary at conserved Tyr(253) for targeting the receptor to the surface.

Amino Acid Motifs↗

PubMed2000

Hormone interactions to Leu-rich repeats in the gonadotropin receptors. II. Analysis of Leu-rich repeat 4 of human luteinizing hormone/chorionic gonadotropin receptor.

The luteinizing hormone receptor (LHR) consists of an approximately 350-amino acid-long N-terminal extracellular exodomain and a membrane-associated endodomain of similar size. Human chorionic gonadotropin (hCG) binds to the exodomain, and then hCG/exodomain complex is thought to make a secondary contact with the endodomain and generate hormone signals. The sequence alignment of the exodomain shows imperfectly matching eight to nine Leu-rich repeats (LRRs). In the preceding article (Song, Y., Ji, I., Beauchamp, J., Isaacs, N., and Ji, T. (2001) J. Biol. Chem. 276, 3426-3435), we have shown that LRR2 and LRR4 are crucial for hormone binding. In this work, we have examined the residues of LRR4, in particular Leu(103) and Ile(105) in the putative beta strand. Our data show that Leu(103) and Ile(105) are involved in the specific, hydrophobic interaction of the LRR4 loop, likely to form the hydrophobic core. This loop is crucial for the structural integrity of all of the LRRs. In contrast, the downstream sequence consisting of Asn(107), Thr(108), Gly(109), and Ile(110) of LRR4 is crucial for cAMP induction but not for hormone binding, folding, and surface expression. This implicates, for the first time, its involvement in the interaction with the endodomain and signal generation. The evidence for the interaction is presented in the following article.

Amino Acid Motifs↗

PubMed2000

Hormone interactions to Leu-rich repeats in the gonadotropin receptors. I. Analysis of Leu-rich repeats of human luteinizing hormone/chorionic gonadotropin receptor and follicle-stimulating hormone receptor.

The luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR) have an approximately 350-amino acid-long, N-terminal extracellular exodomain. This exodomain binds hormone with high affinity and specificity and contains eight to nine putative Leu-rich repeat (LRR) sequences. LRRs are known to assume the horseshoe structure in ribonuclease inhibitors, and the inner lining of the horseshoe consists of the beta-stranded Leu/Ile-X-Leu/Ile motif. In the case of ribonuclease inhibitors, these beta strands interact with ribonuclease. However, it is unclear whether the putative LRRs of LHR and FSHR play any role in the structure and function. In this work, the beta-stranded Leu/Ile residues in all LRRs of the human LHR and FSHR were Ala-scanned and characterized. In addition, the 23 residues around LRR2 of LHR were Ala-scanned. The results show that beta-stranded Leu and Ile residues in all LRRs are important but not equally. These Leu/Ile-X-Leu/Ile motifs appear to form the hydrophobic core of the LRR loop, crucial for the LRR structure. Interestingly, the hot spots are primarily in the upstream and downstream LRRs of the LHR exodomain, whereas important LRRs spread throughout the FSHR exodomain. This may explain the distinct hormone specificity despite the structural similarity of the two receptors.

Alanine↗

PubMed2000

Hormone interactions to Leu-rich repeats in the gonadotropin receptors. III. Photoaffinity labeling of human chorionic gonadotropin with receptor Leu-rich repeat 4 peptide.

Human chorionic gonadotropin (hCG) binds to the extracellular N-terminal domain, exodomain, of its receptor, and the resulting hCG-exodomain complex is thought to modulate the membrane associated domain, endodomain, of the receptor to generate hormone signal. The bulk of the exodomain is speculated to assume a crescent structure consisting of eight to nine Leu-rich repeats (LRRs), which may provide the hormone contact sites. Unfortunately, little experimental evidence is available for the precise hormone contact points in the exodomain and the endodomain. The two preceding articles (Song, Y., Ji, I., Beauchamp, J., Isaacs, N., and Ji, T. (2001) J. Biol. Chem. 276, 3426-3435; Song, Y., Ji, I., Beauchamp, J., Isaacs, N., and Ji, T. (2001) J. Biol. Chem. 276, 3436-3442) show that putative LRR2 and LRR4 are crucial for hormone binding. In particular, the N-terminal region of LRR4 assumes the hydrophobic core of the LRR4 loop, whereas the C-terminal region is crucial for signal generation. However, it is unclear whether LRR4 interacts hCG and the endodomain and how it might be involved in signal generation. In this article, our affinity labeling results present the first evidence that the N-terminal region of LRR4 interacts with hCG, preferentially the hCGalpha subunit and that the hCG/LRR4 complex interacts with exoloop 2 of the endodomain. This interaction offers a mechanism to generate hormone signal.

Amino Acid Motifs↗

PubMed2000

Identification of metabolites of phytosterols in rat feces using GC/MS.

Beta-sitosterol, campesterol and stigmasterol have been known to the phytosterols the most frequently found in plants. Metabolism of phytosterols was investigated using rat feces and liver microsomes. Feces were collected after phytosterols (a well characterized mixture of beta-sitosterol 40%, campesterol 30% and dihydrobrasicasterol) were administered orally (0.5 g/kg) to rats. Metabolites of phytosterols were identified using GC/MS. Three peaks were eluted at 12.47, 12.65, 12.87 min and had characteristic molecular ions m/z 428, 430, 432, respectively. Three fecal metabolites were identified as androstadienedione, androstenedione, and androstanedione. No metabolites could be detected in the rat liver microsomal reaction mixture. The results suggest that the metabolites of phytosterols in rat feces are formed by oxidation at 3- position, saturation at 5- and 6- position, and 17- side chain cleavage in the rat large intestine.

Animals↗

PubMed2000

Analytical procedure for quantifying five compounds suspected as possible contaminants in recycled paper/paperboard for food packaging.

Because contaminants in recycled paper intended for food packaging could be a risk to public health, analytical methods are needed to identify and quantify residues of concern in paper/paperboard. The U. S. Food and Drug Administration is considering development of a guidance document for testing levels of contaminants that might be retained through paper recycling processes. An analytical procedure was developed using paper spiked with suspected contaminants at concentrations of 1-50 ppm in the paper. Benzophenone, dimethyl phthalate, anthracene, methyl stearate, and pentachlorophenol were introduced by soaking the paper in a solution in acetone at 25 degrees C for 24 h; the paper was removed and dried by evaporating the solvent with nitrogen. The model contaminant residues were extracted from the paper using ultrasonication and quantified by GC with flame ionization and electron capture detectors. Recoveries from the spiked paper were 80-109% with a repeatability of +/-4%. The method was also used to analyze commercial recycled paperboard to validate its applicability.

Chromatography, Gas↗

PubMed2000

12-O-tetradecanoyl phorbol 13-acetate, protein kinase C (PKC) activator, protects human leukemia HL-60 cells from taxol-induced apoptosis: possible role for extracellular signal-regulated kinase.

The purpose of this study was to evaluate whether the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) signaling pathway contributes to 12-O-tertadecanoyl phorbol 13-acetate (TPA)-mediated protection from taxol-induced apoptosis of human leukemia HL-60 cells. Treatment of cells with taxol for 12 h resulted in apoptosis of HL-60 cells. TPA was protective against taxol-induced apoptosis and this anti-apoptotic effect was reversible when TPA was used in conjunction with staurosporine and H-7, PKC inhibitors, suggesting that TPA may protect HL-60 cells against taxol-induced apoptosis via the PKC-dependent pathway. Since TPA stimulates MEK signal transduction pathway in HL-60 cells, we postulated that MEK pathway may be playing a role in the ability of TPA to inhibit taxol-induced apoptosis. PD098059, a specific MEK kinase inhibitor, abolished the ability of TPA to inhibit taxol-induced apoptosis. These results suggest that activation of PKC in HL-60 cells confers protection against taxol-induced apoptosis and that MEK mediates anti-apoptotic signaling of PKC.

Antineoplastic Agents, Phytogenic↗

PubMed1999

Social support and unsupportive social interactions: their association with depression among people living with HIV.

Although numerous studies of people living with HIV have focused on positive social support, researchers have directed surprisingly little attention to the nature and effects of negative social interactions in this population. Based on data from a diverse sample of people with HIV (N = 271), we conducted a factor analysis to develop the HIV version of the Unsupportive Social Interactions Inventory (USII). Four types of unsupportive or upsetting responses that an HIV-positive person might receive from others were identified: insensitivity, disconnecting, forced optimism and blaming. In analysis with a sub-sample of 96 people with HIV, unsupportive social interactions were only moderately correlated with social support, suggesting that these constructs are relatively independent. Using hierarchical regression analysis, we found that unsupportive social interactions predicted a significant amount of the variance in depression, beyond the variance accounted for by physical functioning and positive social support. Partial correlations indicated that the relationship between unsupportive social interactions and depression was not an artifact of trait negative affectivity. Favourable evidence of the USII's reliability and validity suggests that the instrument provides a useful tool for assessing unsupportive social interactions experienced by people with HIV. Practical implications of the findings and directions for future research are discussed.

Acquired Immunodeficiency Syndrome↗

PubMed1999

In vitro inducible nitric oxide synthesis inhibitors from Alismatis Rhizoma.

Bioassay-guided fractionation of an aqueous extract of Alismatis Rhizoma has furnished two inducible nitric oxide synthase (iNOS) inhibitory compounds, alismol (1) and alisol B monoacetate (2), together with an inactive triterpene, alisol C monoacetate (3). Compounds 1 and 2 inhibited nitric oxide (NO) synthesis in a dose-dependent manner in murine macrophage-like RAW 264.7 cells stimulated with interferon-gamma (IFN-gamma) plus lipopolysaccharide (LPS). The inhibitory effects of 1 and 2 on NO synthesis were partly due to suppression of iNOS mRNA expression as determined by Northern blotting.

Animals↗

PubMed1999

The loss of expression of transforming growth factor-beta receptors correlates with the histopathologic tumor grade in bladder transitional cell carcinoma patients.

Transforming growth factor-beta (TGF-beta), a pleiotropic growth factor, is a potent inhibitor of cellular proliferation in cells of epithelial origin. Recently, it has been suggested that a loss of sensitivity to TGF-beta through a loss of expression of TGF-beta receptors T beta R-I and T beta R-II--is associated with tumor initiation and progression. Therefore, to investigate the relationship between TGF-beta receptors expression and carcinogenesis of bladder TCC, this study examined the expression of T beta R-I and T beta R-II in 46 bladder TCC patients using immunohistochemistry. Since histopathological grade is a widely accepted marker of prognosis, the results were compared in relation to the three grades of bladder TCC. The results demonstrated that the loss of TGF-beta receptors expression is associated with increasing histopathological grades of bladder TCC. Specifically, both T beta R-I and T beta R-II were readily detected in all 10 normal bladder mucosa specimens. Likewise, all 6 specimens of grade I TCC samples expressed high levels of both TGF-beta receptors. However, among grade II TCC samples, T beta R-I and T beta R-II were detected in 78% and 89%, respectively: among grade III TCC samples, T beta R-I and T beta R-II were detected in 45% and 41%, respectively. These results suggested that loss of sensitivity to TGF-beta may play a role in the progression of TCC from low to high grade disease.

Adult↗

PubMed1998

Induction of late activation events by Igbeta signaling subunit of B-cell receptor in Jurkat T-cell without tyrosine phosphorylation.

T-lymphocyte activation consists of multiple intracellular signaling events, eventually leading to cellular proliferation by the control of cytokine gene expression and the acquisition of diverse effector function. To investigate the functional specificity of ITAM (Immunoreceptor Tyrosine-based Activation Motif), chimeric molecules CD8-zeta, CD8-Igalpha, CD8-Igbeta, which contain the extracellular and transmembrane domains of the human CD8alpha molecule and the cytoplasmic tail of T-cell receptor (TcR) chain, Igalpha or Igbeta subunit of B-cell receptor, respectively, were stably expressed in a Jurkat cell line. Upon stimulation with anti-CD8 mAb OKT8, CD8-zeta and CD8-Igalpha chimeric proteins induced tyrosine phosphorylation of various cytoplasmic substrates as seen in TcR stimulation. They were also capable of stimulating IL-2 gene expression in a NF-AT dependent manner and inducing CD69 expression on the surface. However, stimulation of CD8-Igbeta can induce activation of CD69 surface expression and IL-2 gene expression equivalent to the level by CD8-Igalpha and CD8-zeta without induction of the tyrosine phosphorylation of intracellular signaling molecules. These results suggested that some of signaling chains containing ITAM may utilize a signal pathway without substrate tyrosine phosphorylation during T-cell activation leading to the IL-2 secretion.

Antigens, CD↗

PubMed1998

Genetic integrity of transforming growth factor beta (TGF-beta) receptors in cervical carcinoma cell lines: loss of growth sensitivity but conserved transcriptional response to TGF-beta.

Transforming growth factor beta (TGF-beta) exerts an inhibitory effect on the growth of most epithelial cell types, and the loss of responsiveness to this growth inhibition has been implicated in the development of a variety of human cancers. The genetic alteration of TGF-beta receptors is known to play a critical role in this escape from growth regulation. We asked whether there is a correlation between TGF-beta sensitivity and the genetic status of TGF-beta type I and type II receptors (RI and RII, respectively) in human cervical carcinoma cell lines. Among 8 cell lines examined, 3 (ME-180, C-33A and HeLaS3) showed resistance to TGF-beta and 3 (SiHa, CaSki and HeLa229) showed minimal response to the growth inhibitory effect of TGF-beta; the other cell lines (HeLa and HT-3) were sensitive. Northern blot analysis revealed that the RII mRNA was not expressed in 2 TGF-beta-resistant cell lines (ME-180 and C-33A) but was expressed in the other cell lines. Southern blot analysis of RI and RII revealed a homozygous deletion of the entire TGF-beta RII gene in the cell line ME-180. We then asked whether the other TGF-beta-resistant or refractory cell lines had microsatellite instability and/or poly-adenine tract mutations of RII. We also checked for point mutations in the individual exons of the entire RII using polymerase chain reaction-single-strand conformational polymorphism (PCR-SSCP). Although C-33A exhibited poly-adenine microsatellite instability, its RII gene showed no signs of mutation. The molecular integrity of the TGF-beta, receptors in all cell lines, except ME-180 and C-33A, could be confirmed by examining the distinct transcriptional induction of plasminogen activator inhibitor-1 (PAI-1), p21(WAF1/CIP1) and, in some cases, the accompanying downregulation of c-myc in response to TGF-beta. Our observations, taken together, indicate that inactivation of the RII contributes to the resistance to TGF-beta of some cervical carcinoma cell lines. Loss of or attenuated sensitivity to TGF-beta growth inhibition in other cells may be attributed to the disruption of distal components in the TGF-beta signal pathway, but not to the receptor system.

Blotting, Southern↗

PubMed1998

Identification of antigenic differences between the phosphorylated and nonphosphorylated forms of the E7 protein of human papillomavirus type 16.

To analyze the antigenic properties of the human papillomavirus type 16 E7 oncoprotein, two monoclonal antibodies, VD6 and IB10, that have different reactivities to the E7 protein were generated. While the VD6 antibody reacted strongly with E7 protein in CaSki cell extracts, the other antibody, IB10, showed much weaker reactivity with E7. This reactivity increased in a dose-dependent manner in the presence of the casein kinase II-specific inhibitor DRB (5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole). Antigenic site estimation and an in vitro phosphorylation assay, using bacterially expressed E7 protein, demonstrated that the weak reactivity of IB10 was related to the phosphorylation status of the E7 protein. Phosphorylation of E7 reduced considerably the reactivity of IB10 but did not affect the reactivity of VD6, which reacts with the N-terminal portion of E7. In immunoprecipitation (IP) assays, IB10 precipitated weakly the E7 protein from CaSki cell extracts. Together, these data suggest that unphosphorylated E7 protein shows distinct antigenic character compared to its phosphorylated form under denaturing conditions; however, under native conditions, the phosphorylated and nonphosphorylated E7 proteins have some antigenic cross-reactivity.

Animals↗