Biomedical subjects

Wei Chen

Publications and source records attributed to Wei Chen.

At least 397 records · Page 22Linked to original sources

PubMed2004

[Expression of prostate stem cell antigen (PSCA) and selection of its specific binding peptide].

Prostate stem cell antigen (PSCA), a homologue of the Ly-6/Thy-1 family of cell surface antigen, is expressed by a majority of human prostate cancers and is a promising target for prostate cancer immunotherapy. To obtain the specific peptide binding with PSCA for targeted immunotherapy, PSCA gene was obtained by RT-PCR from human prostate cancer cell line DU145 and the transcated PSCA (tPSCA) gene was cloned into vector pQE30 for soluble expression in E. coli. The identity of recombinant tPSCA was confirmed through ELISA and western blot by use of anti-PSCA monoclonal antibody. Then the 12-peptide phage display library was screened with the purified tPSCA protein for its specific binding peptide through 3 rounds panning. For identifying the peptide's specificity, the peptide was coupled with EGFP (enhanced green fluorecent protein) by recombinant DNA technology and the recombinant coupled protein was termed 11-EGFP. The binding specificity with tPSCA of 11-EGFP was further confirmed by ELISA and competitive inhibition experiment. Flow cytometry demonstrated its binding specificity with cell line DU145. In conclusion, a 12-amino-acid peptide which could bind with PSCA specifically was found and it may be a potential tool for targeted immunotherapy of prostate carcinoma.

Antibodies, Monoclonal↗

PubMed2004

[Construction of CHO-IVB, A serum-independent, apoptosis-resistant cell line that can grow in adherence].

Without serum to provide adherent factors, CHO-dhfr- cells grow in suspension when cultured in serum-free medium. Although this offers advantages in some applications, in most production systems adherent cell growth is preferable. Gene transfection, clonal selection and amplification can be easier for adherent cells; the density of immobilized cells is often higher than those in suspension culture, which results in a higher protein productivity; washout of cells by perfused medium during continuous fermentation can be avoided; for high-throughput microplate assays, adherent cells are preferred to facilitate medium changes and cell washing. It has been proved that purified vitronectin alone was able to mediate attachment and spreading of CHO cells in serum-free medium. So we constructed a tricistronic expression vector expressing Igf-1, Vitronectin and Bel-2 at the same time. The vector was transfected into CHO-dhfr- cells and one clone, namely CHO-IVB2, expressing high level of the three proteins was screened out by Western blot. The cell line showed similar apoptosis-resistant and serum-independent properties to CHO-IB, an engineered cell line constructed before. When cultured in IMEM protein-free medium without any components supplemented, CHO-IVB can grow adherently. The viable cell numbers and growth rate of CHO-IVB were much higher than CHO-IB, making CHO-IVB an apoptosis-resistant host for production of recombinant proteins which can grow adherently in protein-free medium.

Animals↗

PubMed2004

[Construction of two robust CHO cell lines resistant to apoptosis and adapted to protein-free medium by over-expression of Igf-1/bcl-2 or bcl-2/cyclin E genes].

Serum used widely in mammalian cell culture is also a potential source of bacterial, mycoplasmal and viral contaminations. In addition, the complex biological components in serum make harder the subsequent product recovery process. High cost, high batch variation and potential source limitation are among the other shortcomings. So serum-free or even protein-free medium are preferable for recombinant protein production. However, without serum to provide essential components such as hormones, growth factors and binding proteins, cells are easy to die. In this study, CHO-dhfr- cells were genetically engineered to make them adapted to IMEM, a protein-free medium, and resistant to apoptosis. The genes in choice are insulin-like factor (Igf-1), Bcl-2 and cyclin E. Bcl-2 is a mitochondrial membrane-integrated protein. It can block the release of cytochrome c by maintaining the integrity of mitochondrial membrane, and thus inhibit apoptosis. Igf-1 is similar both in structure and function to insulin, a growth factor added to serum-free medium to promote cell growth and is the only protein component in many currently used serum-free media. cyclin E is a cell cycle protein expressed continuously in G1 phase. When cyclin E accumulates to certain amount, cell cycle was driven to S phase. So cyclin E is a proliferation-promoting protein. By co-express Igf-1/Bcl-2 or Bcl-2/ cyclin E in CHO-dhfr- cells with a dicistronic expression vector, we constructed two cell lines: CHO-IB and CHO-BC. The high expression of each protein was confirmed by Western blot and flow cytometry. Apoptosis was analyzed by flow cytometry and DNA ladder detection, and the two cell lines were both found much more resistant to apoptosis induced by withdrawal of serum or addition of actinomycin D than the CHO-dhfr- parent cell. Cell proliferation assay by MTT method showed that the two cell lines proliferated much faster than CHO-dhfr- in IMDM medium without serum. Continuously culture assay proved that the two cell lines grow very well in IMEM protein-free medium supplemented with fibronectin and vitronectin to ease adherence. When compared to CHO-dhfr-, the two cell lines exhibited much more viable cell numbers and faster growth rate.

Animals↗

PubMed2004

[Expression and characterization of the recombination anthrax lethal factor].

The gene encoding anthrax lehtal factor (LF) was cloned into a secretory expression plasmid and then expressed in periplasmic space of E. coli. The recombinant LF (rLF) expressed was about 4% of the total proteins in E. coli. About 3 mg electrophoresis purity rLF could be obtained after the purification of 1 liter culure using ion exchange chromatography and gel filtration. The result of sequencing assay showed that the N-terminal amino acid sequence of rLF was identical to the N-terminal sequence of natural LF. In vitro toxicity analysis also shows that rLF has an excellent biological activity. The successful expression of rLF has placed a solid foundation for the research on toxicity mechanism of LF, developing new anthrax vaccines, and screening for inhibitors against anthrax toxin.

Animals↗

PubMed2003

Efficiency optimization in a correlation ratchet with asymmetric unbiased fluctuations.

The efficiency of a Brownian particle moving in a periodic potential in the presence of asymmetric unbiased fluctuations is investigated. We found that even on the quasistatic limit there is a regime where the efficiency can be a peaked function of temperature, which proves that thermal fluctuations facilitate the efficiency of energy transformation, contradicting the earlier findings [H. Kamegawa et al., Phys. Rev. Lett. 80, 5251 (1998)]. It is also found that the mutual interplay between temporal asymmetry and spatial asymmetry may induce optimized efficiency at finite temperatures. The ratchet is not most efficient when it gives maximum current.

Journal Article↗

PubMed2003

Thrombopoietin cooperates with FLT3-ligand in the generation of plasmacytoid dendritic cell precursors from human hematopoietic progenitors.

Type 1 interferon-producing cells (IPCs), also known as plasmacytoid dendritic cell (DC) precursors, represent the key effectors in antiviral innate immunity and triggers for adaptive immune responses. IPCs play important roles in the pathogenesis of systemic lupus erythematosus (SLE) and in modulating immune responses after hematopoietic stem cell transplantation. Understanding IPC development from hematopoietic progenitor cells (HPCs) may provide critical information in controlling viral infection, autoimmune SLE, and graft-versus-host disease. FLT3-ligand (FLT3-L) represents a key IPC differentiation factor from HPCs. Although hematopoietic cytokines such as interleukin-3 (IL-3), IL-7, stem cell factor (SCF), macrophage-colony-stimulating factor (M-CSF), and granulocyte M-CSF (GM-CSF) promote the expansion of CD34+ HPCs in FLT3-L culture, they strongly inhibit HPC differentiation into IPCs. Here we show that thrombopoietin (TPO) cooperates with FLT3-L, inducing CD34+ HPCs to undergo a 400-fold expansion in cell numbers and to generate more than 6 x 10(6) IPCs per 10(6) CD34+ HPCs within 30 days in culture. IPCs derived from HPCs in FLT3-L/TPO cultures display blood IPC phenotype and have the capacity to produce large amounts of interferon-alpha (IFN-alpha) and to differentiate into mature DCs. This culture system, combined with the use of adult peripheral blood CD34+ HPCs purified from G-CSF-mobilized donors, permits the generation of more than 10(9) IPCs from a single blood donor.

Antigens, CD↗

PubMed2003

Retroviral immunotoxin gene therapy of leukemia in mice using leukemia-specific T cells transduced with an interleukin-3/Bax fusion protein gene.

In past studies, we showed that T cells transduced with retroviral diphtheria immunotoxin (IT) target genes could serve as vehicles for delivering IT to tumors in vivo. We took advantage of the observation that antigen-specific T cells are able to penetrate tumors to design an approach delivering combined cellular and humoral therapy directly to the tumor site. To improve tumor specificity, we selected interleukin (IL)-3 as a ligand because its receptor is selectively overexpressed on myeloid leukemia progenitors. Because Bcl-2 family proteins show structural similarity to diphtheria toxin (DT), we constructed a unique retroviral IT using Bax, a proapoptotic member of the Bcl-2 family, in place of DT. Bax was chosen because several studies showed that its transduction induces lethal apoptosis in different cancers. The retroviral construct for gene therapy included IL-3 positioned downstream of its 80 amino acid leader, and permitted cotranslational protein synthesis of hybrid IL-3/human Bax fusion protein. Other vectors were constructed with IL-3 fused to DT or Pseudomonas exotoxin. Retroviral vectors were used to transiently transduce C8, a CD4(+) T cell clone that specifically recognized FBL-3, a lethal myeloid leukemia. Supernatants collected from transduced cells showed proapoptotic activity and selectively inhibited FBL-3 cells in vitro. Intraperitoneal injection of transduced but not nontransduced C8 into mice with subcutaneous tumors or systemic cancer significantly inhibited tumor growth. These results indicate that retroviral IT made with IL-3 and various toxic proteins may be useful in patients with acute myelogenous leukemia (AML). Furthermore, the Bax construct may be particularly useful as a nonimmunogenic substitute for bacterial toxins in retIT.

Animals↗

PubMed2003

[An epidemiological study on the relationship between selenium and thyroid function in areas with different iodine intake].

OBJECTIVE: To investigate the relationship between selenium status and thyroid dysfunction in 3 areas with different iodine intake. METHODS: An epidemiological research was performed in the rural communities of Panshan County (iodine-deficient area) and Zhangwu County (iodine-sufficient area), Liaoning Province, and Huanghua County, Hebei Province (iodine-excessive area). Serum selenium, TSH, FT3 and FT4 levels were examined in 329 patients with thyroid dysfunction (including clinical hypothyroidism, subclinical hypothyroidism, clinical hyperthyroidism and subclinical hyperthyroidism) and 183 normal inhabitants. RESULTS: The median serum selenium concentrations in Panshan, Zhangwu and Huanghua were 91.4, 89.1, and 83.2 microg/L respectively. There was no difference in serum selenium levels between the patients with subclinical hypothyroidism, clinical hypothyroidism, and clinical hyperthyroidism and their normal controls. The median serum selenium concentration of the subclinical hyperthyroidism patients was 82.6 microg/L, significantly lower than that of the normal controls (87.3 microg/L). The FT3/FT4 ratio was decreased, the FT4 level was increased in the subclinical hyperthyroidism patients in comparison with the normal controls, and no significant difference in FT3 level was found between them. No significant effect of sex and age was found on serum selenium level of normal inhabitants. In normal controls serum selenium was inversely correlated with serum TSH level, and the subjects with serum selenium < or = 80 microg/L had the median TSH level of 2.10 mU/L, markedly higher than that of the subjects with the serum selenium of 80-100 microg/L (1.29 mU/L) and that of the subjects with the serum selenium of 100 approximately 120 micro g/L (1.28 mU/L). For the thyroid dysfunction patients with positive thyroid auto-antibody (TPOAb) in Zhangwu County, the serum selenium was negatively associated with TPOAb level. The serum selenium level of the TPOAb highly positive group (TPOAb > 600 IU/ml) was 83.6 IU/ml, significantly lower than those of the TPOAb lowly positive group and TPOAb moderately positive group (83.6, 92.9 and 95.6 microg/L respectively). CONCLUSION: No obvious effect of selenium status is found on the development of thyroid dysfunction in these three areas. But selenium deficiency can impair thyroid function by means of disturbing thyroid hormone metabolism and decreasing antioxidant ability of the thyroid.

Age Factors↗

PubMed2003

Insulin-like growth factor (IGF)-I/IGF-binding protein-3 complex: therapeutic efficacy and mechanism of protection against type 1 diabetes.

IGF-I regulates islet beta-cell growth, survival, and metabolism and protects against type 1 diabetes (T1D). However, the therapeutic efficacy of free IGF-I may be limited by its biological half-life in vivo. We investigated whether prolongation of its half-life as an IGF-I/IGF binding protein (IGFBP)-3 complex affords increased protection against T1D and whether this occurs by influencing T cell function and/or islet beta-cell growth and survival. Administration of IGF-I either alone or as an IGF-I/IGFBP-3 complex reduced the severity of insulitis and delayed the onset of T1D in nonobese diabetic mice, but IGF-I/IGFBP-3 was significantly more effective. Protection from T1D elicited by IGF-I/IGFBP-3 was mediated by up-regulated CCL4 and down-regulated CCL3 gene expression in pancreatic draining lymph nodes, activation of the phosphatidylinositol 3-kinase and Akt/protein kinase B signaling pathway of beta-cells, reduced beta-cell apoptosis, and stimulation of beta-cell replication. Reduced beta-cell apoptosis resulted from elevated Bcl-2 and Bcl-X(L) activity and diminished caspase-9 activity, indicating a novel role for a mitochondrial-dependent pathway of beta-cell death. Thus, IGF-I/IGFBP-3 affords more efficient protection from insulitis, beta-cell destruction, and T1D than IGF-I, and this complex may represent an efficacious therapeutic treatment for the prevention of T1D.

Animals↗

PubMed2003

Measurement of unidirectional Pi to ATP flux in human visual cortex at 7 T by using in vivo 31P magnetic resonance spectroscopy.

Taking advantage of the high NMR detection sensitivity and the large chemical shift dispersion offered by ultra-high field strength of 7 T, the effect of magnetization transfer on inorganic phosphate (Pi) resonance during saturation of gamma-ATP resonance, mediated by the ATP synthesis reaction, was observed noninvasively in the human primary visual cortex by using in vivo 31P magnetic resonance spectroscopy. The unidirectional flux from Pi to ATP was measured by using progressive saturation transfer experiments. The cerebral ATP synthesis rate in the human primary visual cortex measured by 31P magnetic resonance spectroscopy in this study was 12.1 +/- 2.8 micromol ATP/g per min, which agreed well with the value that was calculated indirectly from the cerebral metabolic rate of glucose consumption reported previously.

Adenosine Triphosphate↗

PubMed2003

Childhood cardiovascular risk factors and carotid vascular changes in adulthood: the Bogalusa Heart Study.

CONTEXT: Carotid artery intima-media thickness (IMT) is associated with cardiovascular risk factors and is recognized as an important predictive measure of clinical coronary atherosclerosis events in middle-aged and elderly populations. However, information on the association of carotid IMT in young adults with different risk factors measured in childhood, adulthood, or as a cumulative burden of each of the risk factors measured serially from childhood to adulthood is limited. OBJECTIVE: To examine the association between carotid IMT in young adults and traditional cardiovascular risk factors measured since childhood. DESIGN, SETTING, AND PARTICIPANTS: A cohort study of 486 adults aged 25 to 37 years from a semirural black and white community in Bogalusa, La (71% white, 39% men), who had at least 3 measurements of traditional risk factors since childhood, conducted between September 1973 and December 1996. MAIN OUTCOME MEASURE: Association of carotid IMT with risk factors, including systolic blood pressure, lipoprotein levels, and body mass index. RESULTS: Male vs female (0.757 mm vs 0.719 mm) and black vs white (0.760 mm vs 0.723 mm) participants had increased carotid IMT (P<.001 for both). In multivariable analyses, significant predictors for being in top vs lower 3 quartiles of carotid IMT in young adults were childhood measures of low-density lipoprotein cholesterol (LDL-C) level (odds ratio [OR], 1.42, corresponding to 1-SD change specific for age, race, and sex; 95% confidence interval [CI], 1.14-1.78) and body mass index (BMI; OR, 1.25; 95% CI, 1.01-1.54); adulthood measures of LDL-C level (OR, 1.46; 95% CI, 1.16-1.82), high-density lipoprotein cholesterol (HDL-C) level (OR, 0.67; 95% CI, 0.51-0.88), and systolic blood pressure (OR, 1.36; 95% CI, 1.08-1.72); and long-term cumulative burden of LDL-C (OR, 1.58; 95% CI, 1.24-2.01) and HDL-C (OR, 0.75; 95% CI, 0.58-0.97) levels measured serially from childhood to adulthood. An increasing trend in carotid IMT across quartiles of LDL-C level measured in childhood was observed, with a mean value of 0.761 mm (95% CI, 0.743-0.780 mm) for those at the top quartile vs 0.724 mm (95% CI, 0.715-0.734 mm) for those in the lower 3 quartiles (P<.001). CONCLUSIONS: Childhood measures of LDL-C level and BMI predict carotid IMT in young adults. The prevention implications of these findings remains to be explored.

Adult↗

PubMed2003

Cyclosporin A impairs dendritic cell migration by regulating chemokine receptor expression and inhibiting cyclooxygenase-2 expression.

Migration of dendritic cells (DCs) into tissues and secondary lymphoid organs plays a crucial role in the initiation of innate and adaptive immunity. In this article, we show that cyclosporin A (CsA) impairs the migration of DCs both in vitro and in vivo. Exposure of DCs to clinical concentrations of CsA neither induces apoptosis nor alters development but does impair cytokine secretion, chemokine receptor expression, and migration. In vitro, CsA impairs the migration of mouse bone marrow-derived DCs toward macrophage inflammatory protein-3beta (MIP-3beta) and induces them to retain responsiveness to MIP-1alpha after lipopolysaccharide (LPS)-stimulated DC maturation, while in vivo administration of CsA inhibits the migration of DCs out of skin and into the secondary lymphoid organs. CsA impairs chemokine receptor and cyclooxygenase-2 (COX-2) expression normally triggered in LPS-stimulated DCs; administration of exogenous prostaglandin E2 (PGE2) reverses the effects of CsA on chemokine receptor expression and DC migration. Inhibition of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) pathway signaling by CsA may be responsible for the CsA-mediated effects on the regulation of chemokine receptor and cyclooxygenase-2 (COX-2) expression. Impairment of DC migration due to inhibition of PGE2 production and regulation of chemokine receptor expression may contribute, in part, to CsA-mediated immunosuppression.

Animals↗

PubMed2003

Dishevelled 2 recruits beta-arrestin 2 to mediate Wnt5A-stimulated endocytosis of Frizzled 4.

Wnt proteins, regulators of development in many organisms, bind to seven transmembrane-spanning (7TMS) receptors called frizzleds, thereby recruiting the cytoplasmic molecule dishevelled (Dvl) to the plasma membrane.Frizzled-mediated endocytosis of Wg (a Drosophila Wnt protein) and lysosomal degradation may regulate the formation of morphogen gradients. Endocytosis of Frizzled 4 (Fz4) in human embryonic kidney 293 cells was dependent on added Wnt5A protein and was accomplished by the multifunctional adaptor protein beta-arrestin 2 (betaarr2), which was recruited to Fz4 by binding to phosphorylated Dvl2. These findings provide a previously unrecognized mechanism for receptor recruitment of beta-arrestin and demonstrate that Dvl plays an important role in the endocytosis of frizzled, as well as in promoting signaling.

Adaptor Proteins, Signal Transducing↗

PubMed2003

Beta-arrestin 2 mediates endocytosis of type III TGF-beta receptor and down-regulation of its signaling.

beta-Arrestins bind to activated seven transmembrane-spanning (7TMS) receptors (G protein-coupled receptors) after the receptors are phosphorylated by G protein-coupled receptor kinases (GRKs), thereby regulating their signaling and internalization. Here, we demonstrate an unexpected and analogous role of beta-arrestin 2 (betaarr2) for the single transmembrane-spanning type III transforming growth factor-beta (TGF-beta) receptor (TbetaRIII, also referred to as betaglycan). Binding of betaarr2 to TbetaRIII was also triggered by phosphorylation of the receptor on its cytoplasmic domain (likely at threonine 841). However, such phosphorylation was mediated by the type II TGF-beta receptor (TbetaRII), which is itself a kinase, rather than by a GRK. Association with betaarr2 led to internalization of both receptors and down-regulation of TGF-beta signaling. Thus, the regulatory actions of beta-arrestins are broader than previously appreciated, extending to the TGF-beta receptor family as well.

Amino Acid Motifs↗

PubMed2003

Synthesis, structure, and photoelectronic effects of a uranium-zinc-organic coordination polymer containing infinite metal oxide sheets.

The hydrothermal reaction of ZnUO2(OAc)4.7H2O with pyridine-2,3-dicarboxylic acid gives rise to a novel uranium-zinc-organic coordination polymer containing infinite U-O-Zn double sheets and organic ligands. Thermal and photoelectrochemical analyses indicate that the coordination polymeric compound not only has a high thermal stability but also exhibits interesting photoelectronic properties.

Journal Article↗

PubMed2003

Measurement of arterial input function of 17O water tracer in rat carotid artery by using a region-defined (REDE) implanted vascular RF coil.

A method of determining arterial input function (AIF) by continuously detecting the (17)O MR signal changes of (17)O-labeled water tracer in the rat carotid artery using a region-defined (REDE) implanted vascular RF coil at 9.4 Tesla is reported. This coil has a compact physical size of 1 mm inner diameter, 3 mm outer diameter and 11 mm in length. It can be readily implanted into the rat neck and wrapped around the rat carotid artery for achieving adequate MR detection sensitivity for determining AIF with minimal surgical trauma. Water phantom and in vivo MR experiments were conducted for validating the coil's performance. A signal-to-noise ratio of approximately 20:1 was achieved for the (17)O signal acquired from naturally abundant H(2)(17)O in a small amount of blood (approximately 7 microl) inside the rat carotid artery with an acquisition time of 11 s. The REDE RF coil design electromagnetically isolates the rat carotid artery from surrounding tissues and ensures that the MR signal detected by the RF coil is only attributable to the artery blood. It also minimizes the electromagnetic coupling between the implanted RF coil and a head surface coil tuned at the same operating frequency (two-coil configuration). This configuration allowed simultaneous measurements of dynamic changes of (17)O MR signal of the H(2)(17)O tracer in both rat carotid artery and brain. Compared to most contemporary MR approaches, the REDE implanted RF provides a simple, accurate, and promising solution for determination of AIF in small experimental animals.

Animals↗

PubMed2003

GIPC interacts with the beta1-adrenergic receptor and regulates beta1-adrenergic receptor-mediated ERK activation.

Beta1-adrenergic receptors, expressed at high levels in the human heart, have a carboxyl-terminal ESKV motif that can directly interact with PDZ domain-containing proteins. Using the beta1-adrenergic receptor carboxyl terminus as bait, we identified the novel beta1-adrenergic receptor-binding partner GIPC in a yeast two-hybrid screen of a human heart cDNA library. Here we demonstrate that the PDZ domain-containing protein, GIPC, co-immunoprecipitates with the beta1-adrenergic receptor in COS-7 cells. Essential for this interaction is the Ser residue of the beta1-adrenergic receptor carboxyl-terminal ESKV motif. Our data also demonstrate that beta1-adrenergic receptor stimulation activates the mitogen-activated protein kinase, ERK1/2. beta1-adrenergic receptor-mediated ERK1/2 activation was inhibited by pertussis toxin, implicating Gi, and was substantially decreased by the expression of GIPC. Expression of GIPC had no observable effect on beta1-adrenergic receptor sequestration or receptor-mediated cAMP accumulation. This GIPC effect was specific for the beta1-adrenergic receptor and was dependent on an intact PDZ binding motif. These data suggest that GIPC can regulate beta1-adrenergic receptor-stimulated, Gi-mediated, ERK activation while having no effect on receptor internalization or Gs-mediated cAMP signaling.

Adaptor Proteins, Signal Transducing↗

PubMed2003

Molecular cloning, developmental expression, promoter analysis and functional characterization of the mouse CNBP gene.

Striking conservation in various organisms suggests that cellular nucleic acid-binding protein (CNBP) plays a fundamental biological role across different species. However, the regulated expression and physiological properties of the CNBP gene are unknown. In this study, we report the molecular cloning, promoter characterization, developmental expression and functional analysis of the mouse CNBP gene. The gene contains five exons and is localized to chromosome 6 in the region corresponding to band 6 D1-D2. Primer extension assay indicates that the transcription start site is located 230 bp upstream of the initiator Met codon. Our promoter analysis indicates that strong transcription enhancer and silencer regions lie within the 1.6 kb proximal region of the promoter and the upstream -3.0 to -1.6 kb region, respectively. The promoter activity is 10 fold higher in embryonic carcinoma cells than that in fibroblast, as determined by CAT assay. Consistent with its function as a transcription factor, CNBP protein is located in the nucleus of cells. During mouse embryogenesis, CNBP is expressed in the anterior region of the early embryo and in the limb, tail and craniofacial region. Overexpression of CNBP strongly stimulates cell proliferation and increases c-myc promoter activity. Our finds suggest that CNBP may play an important role in cell proliferation and tissue patterning during anterior-posterior axis, craniofacial and limb development by targeting c-Myc.

Animals↗