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T Chen

Publications and source records attributed to T Chen.

At least 217 records · Page 12Linked to original sources
PubMed1998

[Hepatitis B virus replication status and its response to surgery for tumor in hepatocellular carcinoma patients with positive markers of HBV].

OBJECTIVE: To investigate the status of hepatitis B virus (HBV) activity in patients with hepatocellular carcinoma (HCC) and its response to surgical interventions for tumor in HBV positive HCC patients. METHOD: We analyzed HBV marker results and detected HBV DNA in sera of 97 HCC patients (pre-operation 66 cases, post-operation 31 cases) with polymerase chain reaction (PCR) assay. We also investigated the HBV DNA titer in sera before and one week after operation in 20 HCC patients with positive HBV markers by quantitative polymerase chain reaction (Q-PCR). RESULT: HBV DNA positive rate in sera was 40.9% and 64.52% in the two subgroup respectively (P < 0.05). HBV DNA titer in sera increased after operation (P < 0.01). CONCLUSION: The infection rate of HBV in Chinese HCC patients is very high. The replication of hepatitis B virus is strong in partial HBV marker positive HCC patients and surgical interventions may promote the virus replication.

Carcinoma, Hepatocellular↗
PubMed1998

Culture and propagation of Hprt mutant T-lymphocytes isolated from mouse spleen.

The optimization of the mouse lymphocyte Hprt mutation assay has been impeded by the relatively poor growth potential of mouse T-cells in vitro, which leads to low cloning efficiencies (CEs) and limited expansion of Hprt mutant clones for molecular analysis of mutations occurring in control and treated mice. In this study, the addition and manipulation of concanavalin A (Con A), mouse interleukin-2 (IL-2), and a commercially available culture supplement, rat T-STIM with Con A, were used to identify growth conditions producing relatively high CEs for mouse T-cells. Supplementation of medium with 10% rat T-STIM, along with appropriate amounts of Con A for priming and exogenous IL-2 for cloning, resulted in average CEs of 15-16% in lymphocytes isolated from spleens of control mice (n = 32) or mice exposed to 1,3-butadiene (n = 27). In addition, several reagents were assessed for their potential to stimulate long-term growth of Hprt mutant clones; these T-cell stimulatory agents included Con A, phytohemagglutinin, and a calcium ionophore ionomycin combined with a tumor promoter phorbol 12-myristate 13-acetate. In a pilot study, stimulation with Con A proved to be the most effective means for propagating mouse T-cell clones under the various conditions tested. In follow-up experiments, transfer of mutant clones to 24-well plates and repeated stimulation with Con A in IL-2 and rat T-STIM supplemented medium was found to expand 76% of 536 mutant clones to about 400,000 to several million cells per clone. These data indicate that rat T-STIM-supplemented medium enhances the initial outgrowth of mouse T-cells, and that repeated mitogenic stimulation with Con A in the presence of IL-2 and rat T-STIM provides a means for propagating mouse T-cell clones for mutation analyses by a variety of methods.

Animals↗
PubMed1997

Analysis of mutations in the K-ras and p53 genes of lung tumors and in the hprt gene of 6-thioguanine-resistant T-lymphocytes from rats treated with 1,6-dinitropyrene.

Direct pulmonary instillation of 1,6-dinitropyrene (DNP) into male Fischer 344 rats results in a dose-dependent induction of lung tumors and 6-thioguanine-resistant (TGr) T-lymphocytes. The treatment also results in DNP binding to dG in the lung and in T-lymphocytes. In the present study, we have examined the types of mutations associated with these responses to DNP. Sequencing of DNA amplification products from 20 DNP-induced lung tumors identified 5 mutations in K-ras codon 12, 4 GGT-->TGT transversions and one GGT-->GAT transition. No mutations were found in K-ras codons 13 or 61. Single-strand conformation polymorphism analysis of p53 exons 5-8 revealed mobility shifts indicative of mutation in 9 of the 20 tumor samples. Eight of the mutations were substitutions at G:C base pairs, and one was a deletion of a single G:C base pair. DNA from 161 TGr lymphocyte colonies cultured from DNP-treated rats was examined for point mutations by amplification of hprt exons 2, 3, and 8, and screening the products for mutant: wild-type heteroduplex formation by denaturing gradient-gel electrophoresis. Only three mutations were found, a G-->T transversion in exon 3, a G-->A transition in exon 8, and a complex mutation consisting of a tandem G-->T transversion and a one base deletion in exon 3. The mutations identified in the DNP-induced lung tumors and TGr T-lymphocytes are consistent with the formation of dG-DNA adducts by DNP. The extremely low recovery of point mutations from TGr lymphocytes suggests that DNP induces a substantial number of mutations by other mechanisms.

Animals↗
PubMed1997

Expression and mutational analysis of the DCC, DPC4, and MADR2/JV18-1 genes in neuroblastoma.

Loss of heterozygosity (LOH) on chromosome 18q21 is found frequently in various human cancers. Three candidate tumor suppressor genes, DCC (deleted in colorectal carcinomas), DPC4 (deleted in pancreatic carcinomas, locus 4), and MADR2/JV18-1 (MAD-related gene 2), have been cloned and identified from this chromosome region. We have reported recently that LOH on chromosome 18q is observed frequently in neuroblastoma. Alterations of DCC are involved in many human tumors. DPC4 and MADR2/JV18-1 are recently demonstrated to be altered in pancreatic and colorectal cancers, respectively. To confirm if inactivation of the DCC, DPC4, and MADR2/JV18-1 genes is involved in the pathogenesis of neuroblastoma and to clarify the mechanism of inactivation, we analyzed the expression of DCC, DPC4, and MADR2/JV18-1 in neuroblastoma cell lines and primary tumors by reverse transcription-PCR and investigated the mutations in the coding regions of these genes by PCR/reverse transcription-PCR single-strand conformation polymorphism. We found that 12 of 25 (48%) cell lines and 14 of 32 (44%) primary tumors, including 3 with 18q LOH, had absent or reduced expression of DCC mRNA. Expression was more likely to be reduced in advanced (67%) than in early stage neuroblastomas (24%) (P = 0.036), suggesting that inactivation of the DCC gene plays an important role in the progression of neuroblastoma. Altered expression of DPC4 was found in six (24%) cell lines and six (19%) tumors. MADR2/JV18-1 expression was reduced or absent only in four (16%) cell lines and three (9%) tumors. Mutations of the DCC genes were examined in 25 of 29 exons in neuroblastoma cell lines, and those exons in which mutations were found were further examined in primary tumors. We found missense mutations of AAC (Asn) to AGC (Ser) at DCC codon 176 in one cell line and ACC (Thr) to ATC (Ile) at codon 1105 in one cell line and tumor, respectively; polymorphisms of CGA (Arg) to GGA (Gly) at codon 201 and TTT (Phe) to TTG (Leu) at codon 951 in most of the cell lines and tumors; and a silent mutation of GAG (Glu) to GAA (Glu) at codon 118 in four cell lines and five primary tumors. We did not identify any mutations in the DPC4 and MADR2/JV18-1 genes in neuroblastoma. Our results suggested that mutations of the DCC gene may be involved in the pathogenesis of neuroblastomas but failed to account for the relatively high frequency of the altered expression, implying that other mechanisms are responsible for the inactivation of the DCC gene in neuroblastoma. Low frequency of reduced or absent mRNA expression and lack of mutations in DPC4 and MADR2/JV18-1 genes suggested a limited role for these two genes in neuroblastoma.

Cell Adhesion Molecules↗
PubMed1997

Several carcinoembryonic antigens (CD66) serve as receptors for gonococcal opacity proteins.

Neisseria gonorrhoeae (GC) is a human pathogen that adheres to and invades genital surfaces. Although pili are required for the initial adherence, the interaction of GC with epithelial cells is also promoted by a family of outer membrane proteins, the opacity (Opa) proteins such as OpaA protein from strain MS11. Studies have demonstrated that the interaction of the OpaA GC with epithelial cells involves binding to heparan sulfate attached to syndecan receptors. However, other Opa proteins interact with CEA gene family member 1 (CGM1) or biliary glycoprotein (BGP), members of the CD66 antigen family. In this study, we demonstrate that, in addition, the 180-kD carcinoembryonic antigen (CEA) is a receptor for Opa proteins. This conclusion was based on the following observations. First, transfected HeLa cells expressing CEA (HeLa-CEA) and the CEA-expressing colon cancer cell line (LS 174T) bound and subsequently engulfed the Opa+ bacteria. These interactions were inhibited by anti-CEA antibody, but could not be inhibited by addition of heparin. Furthermore, OpaI E. coli directly bound purified CEA. We also compared the adherence and invasion by Opa+ bacteria of CD66 transfected HeLa cells: HeLa-BGPa, HeLa-CGM6, HeLa-NCA, HeLa-CGM1a, HeLa-CEA, and HeLa-Neo serving as negative control. Using OpaI as the prototype, the relative ability of the transfected HeLa cell lines to support adherence was (CEA = BGPa >CGM1a >NCA >>CGM6 = Neo). The ability to mediate invasion of the transfectant cells was (CGM1a >CEA >BGPa >NCA >CGM6 = Neo). Among the Opa proteins tested, OpaC proved to be bifunctional, able to mediate adherence to both syndecan receptors and to CD66 antigens.

Animals↗
PubMed1997

Identification of p53 unbound to T-antigen in human cells transformed by simian virus 40 T-antigen.

In several clones of SV40-transformed human cells, we investigated the relative amounts of large T-Antigen (T-Ag) and p53 proteins, both unbound and associated within complexes, with the goal of identifying changes associated with transformation and immortalization. Cells were transformed by wild type (wt) T-Ag, a functionally temperature sensitive T-Ag (tsA58) and other T-Ag variants. Western analysis showed that while most of the T-Ag was ultimately bound by p53, most of the p53 remained unbound to T-Ag. Unbound p53 remained in the supernatant after a T-Ag immunoprecipitation and p53 was present in two to fourfold excess of T-Ag. In one transformant there was five to tenfold more p53 than T-Ag. p53 was present in transformants in amounts at least 200-fold greater than in untransformed human cells. In wt and variant T-Ag transformants, including those generated with tsA58 T-Ag, large amounts of unbound p53 were present in both pre-crisis and immortal cells and when the cells were grown at permissive or non-permissive temperatures. We also found that in transformants produced by tsA58, an SV40/JCV chimeric T-Ag and other variants, T-Ag appeared to form a complex with p53 slowly perhaps because one or both proteins matured slowly. The presence in transformed human cells of large amounts of unbound p53 and in excess of T-Ag suggests that sequestration of p53 by T-Ag, resulting from complex formation, is required neither for morphological transformation nor immortalization of human cells. Rather, these results support the proposal that high levels of p53, the T-Ag/p53 complexes, or other biochemical event(s), lead to transformation and immortalization of human cells by T-Ag.

Antigens, Polyomavirus Transforming↗
PubMed1997

Effect of methacrylic acid:methyl methacrylate monomer ratios on polymerization rates and properties of polymethyl methacrylates.

Five binary formulations were prepared from methyl methacrylate (MMA) and methacrylic acid (MAA) monomers, and six ternary formulations were prepared from polysols of 30% wt polymethyl methacrylate (PMMA)/MMA and MAA. Using thermal analyses (DSC and TGA) the polymerization kinetics, condition of postcuring, relative amount of residual monomers, and glass transition temperature (Tg) were determined. From bar-shaped samples, 25 x 5 x 0.9 mm in dimensions, mechanical properties [flexural moduli (E) and maximum strengths (sigma)] were measured in three-point bending. Polymerization kinetics of binary formulations improved over pure PMMA (from 15 to 4 min) as a result of over a 60-fold increase in propagation-to-termination constants (Kp/Kt) of MAA/MMA. The further addition of PMMA increased the viscosity, slowed down termination, and, consequently, improved the polymerization kinetics twofold. These enhancements occurred without a substantive change in the Tg of the ternary system (ca. 107 degrees C) over pure PMMA (ca. 112 degrees C). Moreover, the Es of the four ternary formulations averaged 2.94 GPa, which was comparable with many values reported in the literature. In contrast the sigma s of these same formulations averaged 97 MPa, which was about 25% better than earlier investigations of pure acrylic. When a thermoplastic material is required for pultruding profiles that cure fast and have good thermal-mechanical properties, ternaries of PMMA/MMA/MAA should be considered.

Biocompatible Materials↗
PubMed1997

Effects of chronic treatment with a cyclic AMP-selective phosphodiesterase inhibitor, rolipram, on excitatory amino acid neurotransmission systems in young and aged rat brains.

Rolipram selectively inhibits cyclic AMP-specific phosphodiesterase, and leads to an increase in cyclic AMP levels in the brain. In this study, we investigated the effects of chronic rolipram treatment on excitatory and inhibitory amino acid neurotransmission systems in young and aged Wistar rat brains. We used in vitro autoradiography with [3H]MK-801, [3H]glycine, D[3H]aspartate, and [3H]muscimol to label N-methyl-D-aspartate (NMDA) receptors, glycine modulatory sites, glutamate transport sites, and gamma-aminobutyric acid-A (GABA) receptors, respectively. Rolipram (0.01 or 0.1 mg/kg, per os) or its vehicle (distilled water) was administered once a day for 4 weeks. The highest binding of [3H]MK-801, [3H]glycine, and D-[3H]aspartate was seen in the hippocampus in vehicle-treated rats. No significant differences in these binding activities were seen between young and aged rat brains. [3H]Muscimol binding was the highest in the cerebellum, and decreased in many brain regions in aged rats. The chronic rolipram treatment resulted in (1) an increase in [3H]MK-801 binding in the dentate gyrus in both young and aged rats, (2) remarkable reductions in D-[3H]aspartate binding in many regions of both young and aged rats, and (3) no or minimal changes in [3H]glycine and [3H]muscimol binding. These results suggest that the chronic rolipram treatment modifies the excitatory amino acid neurotransmission system.

Aging↗
PubMed1997

Rapid identification of Smith-Lemli-Opitz syndrome homozygotes and heterozygotes (carriers) by measurement of deficient 7-dehydrocholesterol-delta 7-reductase activity in fibroblasts.

To extend the enzyme deficiency in Smith-Lemli-Opitz syndrome (SLOS) to extrahepatic tissues, 7-dehydrocholesterol-delta 7-reductase activity was measured in fibroblasts from 10 controls, five SLOS homozygotes, and five obligate heterozygotes. In cells grown almost to confluence in cholesterol-containing medium (4 mg/dL), the conversion of [1,2-3H]7-dehydrocholesterol to cholesterol (7-dehydrocholesterol-delta 7-reductase activity) was 3.8 times higher in control than in homozygote cells and 2.2 times higher than in heterozygote cells. After 24 hours' exposure of the fibroblasts to cholesterol-deficient medium supplemented with lovastatin, 7-dehydrocholesterol-delta 7-reductase activity increased twofold in controls, but did not change significantly in either heterozygous or homozygous cells. In contrast, the activities of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and lathosterol 5-dehydrogenase, two key enzymes that precede 7-dehydrocholesterol-delta 7-reductase in the cholesterol biosynthetic pathway, and low-density lipoprotein (LDL) receptor-mediated binding were equal in control, homozygote, and heterozygote fibroblasts. Further, HMG-CoA reductase activity and LDL receptor-mediated binding increased after exposure of the cells to cholesterol-deficient medium. Fibroblast cholesterol concentrations were approximately equal, although homozygote cells contained 30 times more 7-dehydrocholesterol. Thus, markedly reduced 7-dehydrocholesterol-delta 7-reductase activity that cannot be upregulated after exposure of the cells to cholesterol-deficient medium is diagnostic for the biochemical defect in SLOS. Significantly reduced enzyme activity between the levels in controls and homozygotes without accumulation of 7-dehydrocholesterol in fibroblasts identified heterozygotes.

Fibroblasts↗
PubMed1997

Differences in fibrinolysis and complement inactivation by venom from different northern blacktailed rattlesnakes (Crotalus molossus molossus).

Venom from 72 different Crotalus molossus molossus rattlesnakes was examined for fibrinolysis and for their ability to inactivate human complement. The fibrinolytic activity of the venoms was variable, but smaller (younger) snakes had less fibrinolytic activity than larger (older) snakes. Major differences between the venoms was detected by isoelectric focusing, and reflected in the number and pI of the proteins with fibrinolytic activity. Of the 72 venoms tested, ten had no effect and three had low activity on complement. The rest of the venoms strongly inactivated complement. The snakes with no activity on complement measured 55 cm or less in length, except for one snake which measured 53 cm and completely inactivated complement. Two larger snakes (76 and 84 cm) had a reduced complement-inactivating activity. Some venoms strongly hydrolyzed C2, whereas others had mild or no effect on this complement component. The attack on C3 was variable: some had no effect on C3, while other venoms produced a 125,000 mol. wt protein, which was recognized by antibodies to C3. Only mild hydrolysis of C4 was evident in serum treated with some venoms. No relationship was evident between the venom properties of this species and geographical distribution. Venom variability is an important clinical reality, and is an important consideration when attempting to isolate proteases from this snake species for further study.

Animals↗
PubMed1997

Evaluation of the biocompatibility of a nonceramic hydroxyapatite.

In this study, the biocompatibility of calcium phosphate cement (CPC) was systematically investigated, which included systemic injection acute toxicity assay, cell culture cytotoxicity assay, gene mutation assay (Ames test), chromosome aberration assay (micronucleus test), DNA damage assay (unscheduled DNA synthesis test) and implant histological evaluation. The results showed that the CPC had no toxicity and all tests for mutagenicity and potential carcinogenicity of CPC extracts are negative. CPC was implanted into the femurs of rabbits under no-load condition and the histology of specimens revealed that the implant tightly joined with the surrounding bone, only a very slight histological inflammatory reaction occurred. Thus, CPC is a highly biocompatible material and seems to be safe for application in humans.

Animals↗
PubMed1997

A novel method to measure acoustic speed of bone tissue.

Acoustic speed is an important parameter that can be used to characterize bone tissue for evaluation of osteoporosis. Traditional approaches for measuring acoustic speed require knowledge of either the specimen thickness, which is sometimes difficult to obtain from biological tissues, or the reference fluid velocity that, moreover, is an unknown parameter for internal tissue in in vivo measurement. In this paper, a new method is proposed to measure acoustic speed from dual reflected ultrasound signals. This technique utilizes two transducers placed on the same side of the test object; one for transmitter and receiver, and the other one for receiver only. The acoustic speed of the test object is based on the information of time-of-flight from the signals received by both transducers and the separation distance between the transducer pair. The technique developed here not only eliminates the requirement of knowledge of specimen thickness, but also shows a feasibility for clinical applications. The results of different porcine and bovine bone samples measured in vitro by this technique are in good agreement with those measured by other published methods. In vivo measurement results of 10 healthy young volunteers' tibias are also reported.

Adult↗
PubMed1997

Purification of M5, a fibrinolytic proteinase from Crotalus molossus molossus venom that attacks complement.

Crotalus molossus molossus (northern blacktailed rattlesnake) venom contains agents that affect blood coagulation. A fibrin(ogen)olytic proteinase, called M5, was isolated and purified from this venom by ion exchange chromatography in a two-step procedure. M5 consists of a single non-glycosylated polypeptide chain with a molecular weight of 25 kDa and an isoelectric point of 7.6. It hydrolyses the A alpha and B beta chains of fibrinogen and the alpha and beta chains of fibrin. It also exhibits caseinolytic activity, but has no effect on synthetic substrates cleaved by thrombin, plasmin, kallikrein, or trypsin. The proteolytic activity of the enzyme against fibrinogen, fibrin, and casein is inhibited by ethylenediaminetetraacetic acid (EDTA) and the loss of activity by EDTA treatment can be prevented by addition of Zn2+. This suggests that M5 is a zinc metalloproteinase. M5, at doses of 50 micrograms and higher, induces significant hemorrhage when injected subcutaneously into mice. In addition, it inactivates guinea-pig complement in a dose-dependent fashion and hydrolyses human C2, C3, and C4.

Animals↗
PubMed1997

Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N-(4-hydroxybutyl)nitrosamine.

In a variety of human malignancies, alteration of the p53 tumour suppressor gene is known as a significant indicator of late progression events including invasion and metastasis, with a possible close relationship to genetic instability. Mutational analysis of the p53 and H-ras genes was performed for 10 pairs of N-butyl-N-(4-hydroxybutyl)nitrosamine-induced invasive mouse urinary bladder carcinomas and metastatic foci. p53 Mutations were found in nine of 10 (90%) primary carcinomas and seven of 10 (70%) metastatic foci. A total of eight p53 mutations in primary carcinomas were common in metastatic foci in six pairs. Additional p53 or H-ras mutations which were not identified in the primary carcinomas were found in three metastatic foci. Evaluation of the allelic distribution of the p53 mutations using RT-PCR, PCR and subcloning, further indicated possible intra-tumour genomic heterogeneity or excess copy numbers of the p53 gene due to genetic instability. Overall, p53 alterations were frequent in mouse urinary bladder carcinomas demonstrating progression. The results suggest that genetic instability might underlie generation of additional genetic alterations in this animal model.

Animals↗
PubMed1997

Carcinogenicity of methylurea or morpholine in combination with sodium nitrite in rat multi-organ carcinogenesis bioassay.

For carcinogenic risk assessment of combinations of N-nitroso precursors in man, the effects of feeding methylurea (MU) or morpholine (Mor) plus sodium nitrite (NaNO2) were investigated using a multi-organ carcinogenesis model. In experiment 1, to initiate multiple organs, groups of 10 or 20 male F344 rats were treated with 6 carcinogens targeting different organs. Starting a week after completion of this initiation phase, animals were given 0.1% MU or 0.5% Mor in their food and/or 0.15% NaNO2 in their drinking water for 23 weeks. The induction of tumors and/or preneoplastic lesions in the forestomach and esophagus was significantly increased in the group receiving MU plus NaNO2. The numbers and areas of liver glutathione S-transferase placental form (GST-P)-positive foci were significantly elevated with MU or Mor plus NaNO2. Experiment 2 was conducted to assess formation of N-nitroso compounds in the stomach, and to detect DNA adduct generation in target organs by immunohistochemical staining. Groups of 5 or 14 animals were starved overnight, then given 0.4% MU or 2.0% Mor in the diet, or basal diet alone for 1 h. Then NaNO2 or distilled water was given intragastrically. The mean gastric N-methyl-N-nitrosourea yield in the MU plus NaNO2 group was 7700 micrograms at 2 h after combined administration. The mean N-nitrosomorpholine yield in the group given Mor plus NaNO2 was 6720 micrograms. Immunohistochemically, N7-methyldeoxyguanosine-positive nuclei were evident in the forestomach epithelium at 8 h after the combination treatment with MU plus NaNO2.

Administration, Oral↗
PubMed1997

A simultaneous negative and positive selection method that can detect chimerism at a frequency of 1 per 10,000 by flow cytometry.

A three-color flow cytometric method with a simultaneous negative and positive selection (SNAPS) approach has been developed to detect blood chimerism using a FITC-conjugated recipient-specific HLA monoclonal antibody, a biotinylated donor-specific HLA monoclonal antibody and Cy5-PE-conjugated streptavidin and a PE-conjugated CD3 monoclonal antibody. Detection of simulated blood chimerism at a frequency of 0.01% was achieved by SNAPS. In contrast, by one-color flow cytometry methods, chimerism can be detected at only about 3-4% with the same donor-specific HLA monoclonal antibody. The percentages of donor CD3 cells detected by SNAPS are proportional to the percentages of donor CD3 cells counted. SNAPS method provides a fast, sensitive and reliable way to analyze trace amounts of donor cells in a recipient's blood.

Animals↗
PubMed1997

Self-association of the single-KH-domain family members Sam68, GRP33, GLD-1, and Qk1: role of the KH domain.

Sam68 is a member of a growing family of proteins that contain a single KH domain embedded in a larger conserved domain of approximately 170 amino acids. Loops 1 and 4 of this KH domain family are longer than the corresponding loops in other KH domains and contain conserved residues. KH domains are protein motifs that are involved in RNA binding and are often present in multiple copies. Here we demonstrate by coimmunoprecipitation studies that Sam68 self-associated and that cellular RNA was required for the association. Deletion studies demonstrated that the Sam68 KH domain loops 1 and 4 were required for self-association. The Sam68 interaction was also observed in Saccharomyces cerevisiae by the two-hybrid system. In situ chemical cross-linking studies in mammalian cells demonstrated that Sam68 oligomerized in vivo. These Sam68 complexes bound homopolymeric RNA and the SH3 domains of p59fyn and phospholipase Cgamma1 in vitro, demonstrating that Sam68 associates with RNA and signaling molecules as a multimer. The formation of the Sam68 complex was inhibited by p59fyn, suggesting that tyrosine phosphorylation regulates Sam68 oligomerization. Other Sam68 family members including Artemia salina GRP33, Caenorhabditis elegans GLD-1, and mouse Qk1 also oligomerized. In addition, Sam68, GRP33, GLD-1, and Qk1 associated with other KH domain proteins such as Bicaudal C. These observations indicate that the single KH domain found in the Sam68 family, in addition to mediating protein-RNA interactions, mediates protein-protein interactions.

Adaptor Proteins, Signal Transducing↗