Proteins responsible for fruit allergies in the northwest of Spain

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Psoriasis ungueal: estudio en 661 pacientes con psoriasis vulgar / Nail Psoriasis in Individuals With Psoriasis Vulgaris: A Study of 661 Patients

Introducción y objetivos: La psoriasis ungueal afecta a un número importante de pacientes con psoriasis. No obstante, son raros los estudios epidemiológicos que recojan las características de estos individuos. Describimos la epidemiología y principales características de los pacientes con psoriasis ungueal. Material y método: Se trata de un estudio prospectivo de casos y controles realizado en el Hospital Universitario Marqués de Valdecilla y Hospital Universitario Central de Asturias entre enero de 2007 y diciembre de 2009.ResultadosDe un total de 661 pacientes la psoriasis ungueal fue diagnosticada en el 47,4% de los pacientes. La prevalencia fue 13,5 puntos mayor en hombres que en mujeres. Los pacientes con afectación ungueal presentan mayor severidad de la enfermedad (PASI 12,82 vs 8,22), mayor duración de la misma (20,30 vs 13,94 años), incidencia superior de artropatía psoriática (29,7% vs 11,5%), mayor frecuencia de antecedentes familiares positivos (53,7% vs 42,8%) y mayor proporción de obesidad IMC > 30 (31,6vs 23,9%). La psoriasis en el grupo con afectación ungueal se inicia de forma precoz (74,1 vs 65,5%) y se asocia con menor frecuencia a Cw*0602 (33 vs 50,3%). Conclusiones: La afectación ungueal es una manifestación frecuente en los pacientes con psoriasis y se asocia a mayor gravedad de la enfermedad y mayor número de comorbilidades (AU)

Background and objectives: The nails are affected in a substantial number of patients with psoriasis. Nevertheless, few epidemiological studies have reported the characteristics of patients with nail psoriasis. Here we describe the epidemiology of nail psoriasis and the main characteristics of affected patients. Patients and methods: We undertook a prospective case–control study at Hospital Universitario Marqués de Valdecilla and Hospital Universitario Central de Asturias in Spain between January 2007 and December 2009. Results: Of a total of 661 patients included, 47.4% were diagnosed with nail psoriasis, which was 13.5% more prevalent in men. The group of patients with nail disease had more severe psoriasis (12.82 vs 8.22 points on the psoriasis area and severity index) and a longer disease duration (20.30 vs 13.94years), and included a larger percentage of patients with psoriatic arthritis (29.7% vs 11.5%), a positive family history of the disease (53.7% vs 42.8%), and a body mass index greater than 30 (31.6% vs 23.9%). A larger percentage of the patients with nail disease had early-onset psoriasis (74.1% vs 65.5%) and fewer were carriers of the human lymphocyte antigen Cw*0602 allele (33% vs 50.3%). Conclusions: Nail disease is frequent in psoriasis and is associated with greater severity of psoriasis and a larger number of comorbidities (AU)

[Nail psoriasis in individuals with psoriasis vulgaris: a study of 661 patients]. / Psoriasis ungueal: estudio en 661 pacientes con psoriasis vulgar.

BACKGROUND AND OBJECTIVES: The nails are affected in a substantial number of patients with psoriasis. Nevertheless, few epidemiological studies have reported the characteristics of patients with nail psoriasis. Here we describe the epidemiology of nail psoriasis and the main characteristics of affected patients. PATIENTS AND METHODS: We undertook a prospective case-control study at Hospital Universitario Marqués de Valdecilla and Hospital Universitario Central de Asturias in Spain between January 2007 and December 2009. RESULTS: Of a total of 661 patients included, 47.4% were diagnosed with nail psoriasis, which was 13.5% more prevalent in men. The group of patients with nail disease had more severe psoriasis (12.82 vs 8.22 points on the psoriasis area and severity index) and a longer disease duration (20.30 vs 13.94years), and included a larger percentage of patients with psoriatic arthritis (29.7% vs 11.5%), a positive family history of the disease (53.7% vs 42.8%), and a body mass index greater than 30 (31.6% vs 23.9%). A larger percentage of the patients with nail disease had early-onset psoriasis (74.1% vs 65.5%) and fewer were carriers of the human lymphocyte antigen Cw*0602 allele (33% vs 50.3%). CONCLUSIONS: Nail disease is frequent in psoriasis and is associated with greater severity of psoriasis and a larger number of comorbidities.

Effect of killer immunoglobulin-like receptors in the response to combined treatment in patients with chronic hepatitis C virus infection.

Killer immunoglobulin-like receptors (KIRs) are related to the activation and inhibition of NK cells and may play an important role in the innate response against infection with viruses such as hepatitis C virus (HCV). We examined whether the different combinations of KIRs with their HLA class I ligands influenced the response to combined treatment (pegylated alpha interferon and ribavirin) of patients infected by HCV. A total of 186 consecutive patients diagnosed with chronic HCV infection were analyzed. Seventy-seven patients exhibited HCV RNA levels at 6 months posttreatment and were called nonresponders (NR), while 109 cleared viral RNA and were named sustained viral responders (SVR). Patients were typed for HLA-B, HLA-Cw, KIR genes, and HCV genotype. In our study, the frequency of the KIR2DL2 allele was significantly increased in NR (P < 0.001; odds ratio [OR] = 1.95), as was the frequency of the KIR2DL2/KIR2DL2 genotype (P < 0.005; OR = 2.52). In contrast, the frequencies of the KIR2DL3 genotype (P < 0.001) and KIR2DL3/KIR2DL3 genotype (P < 0.05; OR = 0.54) were significantly increased in the SVR. Different combinations of KIR2DL2 and KIR2DL3 alleles with their ligands were analyzed. The frequency of the KIR2DL2/KIR2DL2-HLA-C1C2 genotype was significantly increased in the NR (P < 0.01; OR = 3.15). Additionally, we found a higher frequency of the KIR2DL3/KIR2DL3-HLA-C1C1 genotype in the SVR group (P < 0.05; OR = 0.33). These results were not affected by the HCV genotype. In conclusion, patients who carried the KIR2DL2/KIR2DL2-HLA-C1C2 genotype were less prone to respond to treatment. However, the KIR2DL3/KIR2DL3-HLA-C1C1 genotype clearly correlated with a satisfactory response to treatment, defined by the clearance of HCV RNA.

Genetic influence of the nonclassical major histocompatibility complex class I molecule MICB in multiple sclerosis susceptibility.

It has been widely reported that the major histocompatibility complex (MHC) class II region provides the main genetic contribution to multiple sclerosis (MS) susceptibility. However, recent studies have suggested that the MHC class I region may also contribute to the development of MS. In this study, we investigated the possible association of the human leukocyte antigen (HLA)-B, MHC class I chain-related gene B (MICB) and MHC class I chain-related gene A (MICA) genes, located in the MHC class I region, with MS susceptibility. For this purpose, we analyzed the distribution of HLA-DR, HLA-B, MICB and MICA alleles in 121 MS patients and 156 healthy controls. Neither HLA-B nor MICA alleles were found to be associated with MS susceptibility, and only the frequency of HLA-DRB1*01 allele was found to be increased in controls (31% vs 14%, P(c) = 0.011). However, MICB*004 allele frequency was significantly increased in MS patients (46.3% vs 23.3%, P(c) < 0.001, odds ratio = 2.82, 95% confidence interval = 1.68-4.73). Although, MICB*004 and HLA-DRB1*15 belong to the AH 7.1 ancestral haplotype, the association of MICB*004 to MS susceptibility was found to be independent of HLA-DRB1*15 in our population. This and previous studies clearly suggest that the MHC class I, in addition to class II, could be involved in MS susceptibility.

Speed and selection in the evolution of killer-cell immunoglobulin-like receptors.

The killer-cell immunoglobulin-like receptors (KIR) form a diverse family of receptors that control the functions of natural killer cells. Sequencing of KIR from primates has revealed the unexpected extent to which this gene family has diversified mostly likely in response to pathogens and to pathogen-mediated selection of their MHC class I ligands. Human KIR diversity is now a burgeoning area for disease association studies. This review examines the evolution of KIR from a primate-centric view in order to rationalize our current knowledge of the diversity of human KIR.

[CARD15 mutations are poorly related to Crohn's disease phenotypes in Asturias]. / Las mutaciones del gen CARD15 presentan escasa relación con los fenotipos de la enfermedad de Crohn en Asturias.

BACKGROUND: the association between the three common CARD15 gene mutations (R702W, G908R, L1007fs) and the genetic susceptibility to Crohn s disease (CD) have been confirmed by several studies, with some differences found, in relation to geographic areas and ethnic groups. OBJECTIVES: To analyze the prevalence of CARD15 gen and its polymorphisms in patients with CD in Asturias and its possible correlation with the different genotypes of the disease. METHODS: a total of 216 CD patients recruited from Asturias (North of Spain) and 86 ethnically matched healthy controls, were typed using Hybprobes on a LightCycler instrument for CARD15 mutations. Patients were subdivided according to Vienna classification. We have studied the frequency of these mutations in the different subgroups of CD patients and analyzed its contribution to the disease clinical characteristics and progression. RESULTS: carrier frequencies for CARD15 mutations in our CD patients were similar to controls (17.8 vs. 17.4%) respectively (NS). CD patients exhibited frequencies of 8.8, 3.0 and 6.0% for the R702, G908R and L1007fs polymorphisms respectively, whereas our control population had allele frequencies of 11.6, 2.3 and 3.5% for the three mutations respectively (NS). We did not find any relationship between CARD15 mutations and the different phenotypes of Crohn s disease, according to Vienna classification. CONCLUSIONS: in our CD population, other factors (i.e. environmental), in addition to genetics, must be mainly involved in the development of the disease.

Las mutaciones del gen CARD15 presentan escasa relación con los fenotipos de la enfermedad de Crohn en Asturias / CARD15 mutations are poorly related to Crohn´s disease phenotypes in Asturias

Introducción: la asociación entre las mutaciones del genCARD15 y la susceptibilidad genética para la enfermedad deCrohn (EC) se ha confirmado en diversos estudios, con ampliasvariaciones observadas a nivel mundial, tanto geográficas comoétnicas.Objetivos: analizar la prevalencia de gen CARD 15 y sus polimorfismosen pacientes con EC en Asturias y su posible correlacióncon los diversos fenotipos de la enfermedad.Métodos: estudiamos la frecuencia de las tres mutaciones delgen CARD15 (R702W, G908R, L1007fs) usando cebadores específicos,en un total de 216 pacientes con EC y 86 controlesprocedentes del área de Oviedo. Los pacientes fueron clasificadosde acuerdo con la edad al diagnóstico, localización la enfermedady su comportamiento clínico (clasificación de Viena).Resultados: la frecuencia global de portadores de las mutacionesdel gen CARD15 en los pacientes con EC fue del 17,3%frente a un 17,6% en controles (NS). Al analizar separadamentelos polimorfismos R702, G908R y L1007fs los pacientes mostrabanfrecuencias del 8,8, 3 y 6% respectivamente, mientras quelos controles las presentaban en el 11,6, 2,3 y 3,5%, sin encontrardiferencias significativas para ninguna de ellas (NS). Las frecuenciasobservadas en controles, fueron similares a las encontradasen otras regiones españolas.Conclusiones: la prevalencia de mutaciones en CARD15 enpacientes con EC en Asturias es menor a la reportada en otrostrabajos publicados en población española. Otros factores ambientales,además de los genéticos, parecen tener mayor importanciaen el desarrollo de EC en nuestra área

Background: the association between the three commonCARD15 gene mutations (R702W, G908R, L1007fs) and the geneticsusceptibility to Crohn’s disease (CD) have been confirmedby several studies, with some differences found, in relation to geographicareas and ethnic groups.Objectives: To analyze the prevalence of CARD15 gen andits polymorphisms in patients with CD in Asturias and its possiblecorrelation with the different genotypes of the disease.Methods: a total of 216 CD patients recruited from Asturias(North of Spain) and 86 ethnically matched healthy controls, weretyped using Hybprobes on a LightCycler instrument for CARD15mutations. Patients were subdivided according to Vienna classification.We have studied the frequency of these mutations in thedifferent subgroups of CD patients and analyzed its contributionto the disease clinical characteristics and progression.Results: carrier frequencies for CARD15 mutations in ourCD patients were similar to controls (17.8 vs. 17.4%) respectively(NS). CD patients exhibited frequencies of 8.8, 3.0 and 6.0% forthe R702, G908R and L1007fs polymorphisms respectively,whereas our control population had allele frequencies of 11.6,2.3 and 3.5% for the three mutations respectively (NS).We did not find any relationship between CARD15 mutationsand the different phenotypes of Crohn’s disease, according to Viennaclassification.Conclusions: in our CD population, other factors (i.e. environmental),in addition to genetics, must be mainly involved in thedevelopment of the disease

The relationship of anti-MICA antibodies and MICA expression with heart allograft rejection.

The role of MICA antibodies in acute heart allograft rejection was examined utilizing 190 pre- and post-transplant serum samples from 44 patients collected during the first year after transplantation. MICA antibodies were detected by CDC test on recombinant cell lines and by the newly developed Luminex MICA antibody detection assay. Additionally, MICA expression was analyzed by 'real time' RT-PCR and by immunohistochemistry in 10 endomyocardial biopsies. Only two subjects had HLA antibodies post-transplant. Nevertheless, MICA antibodies were found in a significant number of subjects. The prevalence of MICA antibodies was significantly higher among those with severe acute rejection (AR) than in those without rejection (60.7% vs. 14.3%, p = 0.0038 by CDC; 55.5% vs. 5.7%, p = 0.0020 by Luminex). In most cases, the appearance of MICA antibodies post-transplant precedes AR. Following transplantation, MICA up-regulation correlated with histological evidence of severe rejection. Monitoring for MICA antibodies post-transplant may be useful to establish new risk factors for acute rejection.

MHC class I chain-related gene B (MICB) is associated with rheumatoid arthritis susceptibility.

OBJECTIVES: Several recent studies have shown that the MHC class III region, located telomeric to HLA-DRB1, contains an additional genetic factor that predisposes to rheumatoid arthritis (RA). In this study, we investigate whether inhibitor of kappaB-like (IkappaBL), MICB or MICA located in the MHC class III region are the second susceptibility gene associated with RA. METHODS: A total of 154 healthy controls and 140 RA patients were genotyped for HLA-DRB1, MICA, MICB and the polymorphism -62 of the IkappaBL gene. RESULTS: A significant increase of HLA-DRB1 shared epitope (SE) alleles was detected in RA patients (61.4 vs 43.5%, P(c) = 0.01, OR = 2.1, 95% CI = 1.3-3.3). Among SE alleles, the HLA-DRB1*0401 (13.5 vs 5.1%, P(c) = 0.04, OR = 3.2, 95% CI = 1.3-8.1) and HLA-DRB1*0404 (6.4 vs 1.2%, P = 0.02, P(c) = NS) showed the most significantly association with RA. No increase of risk was associated with HLA-DRB1*01. Remarkably, the allele MICB*004 was also significantly associated with RA susceptibility (40.7 vs 23.3%, P(c) = 0.01, OR = 2.2, 95% CI = 1.3-3.7). MICB*004 was in linkage disequilibrium with HLA-DRB1*0404 (lambda(s) = 0.33) and HLA-DRB1*0405 (lambda(s) = 0.34). However, MICB*004 was also increased in HLA-DRB1 SE negative patients (37 vs 21.5%, P = 0.04). No significant association between IkappaBL and MICA with RA was found. CONCLUSIONS: MICB*004 allele was associated with RA susceptibility. This allele was in linkage disequilibrium with HLA-DRB1*0404 and DRB1*0405. The association of MICB with RA susceptibility and the functional role of MIC genes in the pathogenesis of RA converts MICB into a candidate to be an additional MHC gene associated with RA susceptibility.

Clinical behavior of multiple sclerosis is modulated by the MHC class I-chain-related gene A.

It is well known that certain HLA class II alleles confer an increased risk for developing multiple sclerosis (MS). Recent studies have suggested HLA class I as a region that may also contribute to the development of MS. In this study, we investigated the association between HLA-DR, HLA-B alleles, and major histocompatibility complex (MHC) class I-chain-related gene A (MICA) transmembrane (MICA-TM) polymorphisms and disease progression in 104 MS patients and 116 healthy controls. DR1 was found to be decreased in patients when compared with controls (p(c) = 0.012). Neither HLA-B nor HLA-DR alleles were found to be associated with MS susceptibility. Furthermore, the prevalence of MICA-A5 in patients with relapsing MS was 9% while the prevalence in progressive forms was 42% (p(c) = 0.0015). The extended haplotypes related to MICA-TM5 that were found in our population were DR7-MICA5-B64 (EH 64.1, delta(s) = 0.38), DR4-MICA5-B62 (EH 62.1, delta(s) = 0.28), and DR11-MICA5-B35 (EH35.1, delta(s) = 0.10), but none of them were found to be associated to MS susceptibility or disease progression. Our data could indicate a possible role of MICA-TM in MS prognosis.

The amino acid at position 97 is involved in folding and surface expression of HLA-B27.

HLA-B27 confers susceptibility to ankylosing spondylitis (AS) but the mechanism linking this association remains unknown. Other properties unrelated to its natural role of antigen presenting function may be important in disease pathogenesis. We determined here the impact of N97D substitution on the folding and expression of HLA-B*2704 transfected in the 721.221 cell line. The mutation at position 97 abolishes the surface expression of non-conformational (HC10) and conformational (ME1) forms. The expression of ME1 forms was found to be absent in B*2704 N97D by immunoprecipitation and flow cytometry of fixed and permeabilized cell experiments with the conformation-sensitive ME1 antibody. However, immunoblotting cell lysates with HC10 revealed the presence of unfolded heavy chain (HC) and HC-dimer forms. The impact of the N97D mutation in the exit from the endoplasmic reticulum (ER) was analysed by western blot after endoglycosidase-H treatment, and it was found that B*2704 N97D was retained and accumulated as unfolded molecules. We tested for mutant association with transporter associated with antigen processing (TAP), calnexin (CNX), calreticulin (CLR) and beta2 microglobulin (beta2m). The wild-type B*2704 and N97D mutants were associated with TAP, CNX and CLR, although HC10 forms of mutant N97D interact more weakly with TAP. Only folded molecules of HLA-B*2704 were associated with beta2m. Surprisingly, the peptide-binding assay demonstrated the ability of unfolded N97D molecules to bind high-affinity peptides. It has been suggested that AS may arise because of aberrant folding of HLA-B27 molecules within the ER. Future work must therefore aim to clarify the functional connection between the unfolded protein response pathway in response to the accumulation of HLA-B27 in the ER. This mutant could be useful as a model for the misfolding of HLA-B27.

Interaction between KIR3DL1 and HLA-B*57 supertype alleles influences the progression of HIV-1 infection in a Zambian population.

KIR and HLA loci are both highly polymorphic, and some HLA class 1 products bind and trigger cell-surface receptors specified by KIR genes. We examined whether KIR genes act in concert with HLA-B locus to control HIV-1 infection in a sample of Zambian patients. DNA samples from 88 Zambian patients with HIV-1 were examined. Patients were classified as either slow progressors (SP; n = 54) or rapid progressors (RP; n = 34) to AIDS. All were typed for HLA-B and KIR genes. Our results reveal an association between B*57 supertype (B*57s, which includes B*57 and B*58 alleles) and delayed progression to AIDS (p = 0.0007 by pc = 0.015; OR = 5.25). We also observed an increase incidence of Bw4-I80 in patients with slow progression (p = 0.001 by pc = 0.003, OR = 5). This increase was found to be secondary to B*57s. The presence of both KIR3DL1 and B*57S has a significant effect on progression to AIDS (p = 0.0008; OR = 5.61). B*57s genotypes with another HLA-B allele different from those in the trans position, which also had a specificity different to Bw4-I80 (Bw4-T80 or Bw6), was also greater in the SP than in the RP group (p = 0.00003; OR = 10.11). The presence of the inhibitory allele KIR3DL1 in combination with the HLA-B*57s alleles that contain the Bw4-I80 epitope, has a highly protective effect against progression to AIDS in Zambian patients.

The HLA-B*5703 allele confers susceptibility to the development of spondylarthropathies in Zambian human immunodeficiency virus-infected patients with slow progression to acquired immunodeficiency syndrome.

OBJECTIVE: To analyze the HLA distribution in a population of individuals from Zambia in order to establish a possible relationship between the progression of human immunodeficiency virus (HIV) infection and the development of spondylarthropathy (SpA). METHODS: A large epidemiologic analysis of rheumatology patients living in Zambia was performed in order to identify those who had SpA. We selected 64 patients with SpA and found that 54 also had HIV type 1 (HIV-1) infection; only 10 were HIV negative. Additionally, we selected 57 HIV-infected individuals without SpA and 43 healthy controls. Among all of the HIV-1-infected patients, 25 SpA-positive and 24 SpA-negative patients were classified as slow progressors to acquired immunodeficiency syndrome (AIDS), and 8 SpA-positive and 26 SpA-negative patients were classified as rapid progressors. All patients were typed for HLA-B alleles. RESULTS: Of the 64 patients with SpA, HIV infection was observed in 54 (84%). The frequency of B*5703 was increased in patients who were SpA positive and HIV positive compared with patients who were SpA negative and HIV positive (P = 0.0002, odds ratio [OR] 8.28). Among patients who were slow progressors to AIDS, this allele was overrepresented in those with SpA compared with those without SpA (corrected P = 0.001, OR 26.25). CONCLUSION: HLA-B*5703 seems to be a protective allele against the progression of HIV infection but could influence the increased incidence of SpA observed in this population.

HLA class I variation in the West African Pygmies and their genetic relationship with other African populations.

We have studied the polymorphism of HLA class I in two West African Pygmy populations, namely, the Bakola from Cameroon and the Mbenzele from the Central African Republic. A unique number of HLA alleles and haplotypes showed specific patterns of these populations. In this study, we identify two alleles (B*37, B*41) and three haplotypes (A*30-B*37, A*66-B*41 and A*68-B*58) that appear to be 'private' or typical of Western Pygmies. These data reflect similarities with the AKA Pygmies from the Central African Republic. On the other hand, we failed to identify alleles that are found at high frequencies among other sub-Saharan populations (B*42, B*51). Allelic and haplotypic frequency distributions show differences between the two Pygmy groups, e.g. B*35 was very common in the Mbenzele but has been found to be absent in the Bakola. In contrast, B*53, which is found in the Bakola, has been found to be rare in the Mbenzele Pygmies. In order to analyse the genetic relationships of the Bakola and Mbenzele Pygmies with other sub-Saharan populations, HLA gene frequencies were subjected to the Neighbour-Joining tree analysis. The Mbenzele, Bakola and AKA were found to be relatively close to each other and isolated from other sub-African populations. However, both the genetic distances and the within-group variation suggests that the Bakola are more admixed with Bantu farmers than Mbenzele.

Psoriasis vulgaris and psoriatic arthritis share a 100 kb susceptibility region telomeric to HLA-C.

OBJECTIVE: To map the locus for susceptibility to psoriasis in patients with psoriatic arthritis. METHODS: Seventy-four patients with psoriatic arthritis and 95 patients with psoriasis vulgaris were included in this study. Polymorphic genes and microsatellite markers centromeric (C1_2_5) and telomeric (C1_4_4, OTF3, HCR and the corneodesmosin gene) to HLA-C were studied in an association analysis. Typing was also performed on a control population of 104 matched donors. RESULTS: The allele Cw*0602 was associated both with psoriasis [49 vs 21%, Pc<0.0003; odds ratio (OR)=3.6, aetiological factor (AF)=0.72] and with psoriatic arthritis (62 vs 21%, Pc<0.000001; OR=6.1, AF=0.83). In psoriatic patients a susceptibility region telomeric to HLA-C that includes C1_4_4 (56 vs 22%, Pc<0.0002; OR=4.39, AF=0.77), OTF3 (85 vs 60%, Pc<0.0002; OR=3.7, AF=0.73) and HCR (63 vs 26%, Pc<0.00001; OR=3.8, AF=0.74) was observed. In psoriatic arthritis patients the susceptibility region was delimited by HLA-C and C1_4_4 (384 allele, 56 vs 22%, Pc<0.0002; OR=4.37, AF=0.77). CONCLUSIONS: Comparing the susceptibility regions associated with the two diseases, an overlapping interval of 100 kb between HLA-C and OTF3, which might contain the psoriasis gene, can be defined.

Cloning and characterization of human complement component C7 promoter.

To study the transcriptional regulation of the human complement component C7, a 1 kb promoter fragment was cloned and the transcription start site was determined. C7 is expressed by the hepatoma-derived cell line Hep-3B, but not by Hep-G2. Transfection of these cell lines with different C7 promoter-luciferase constructs demonstrated that 1 kb of the 5'-flanking region contains the necessary elements for driving C7 transcription in a tissue-specific manner and showed that the sequence between -29/+102 retained the majority of C7 promoter activity in Hep-3B. Electrophoretic mobility shift assays suggested that the binding of the C/EBPalpha transcription factor to a C/EBP sequence located at +42 is essential for C7 expression. To investigate whether the absence of C/EBPalpha expression in Hep-G2 cells is responsible for the lack of C7 transcription, Hep-G2 cells were transfected with a C/EBPalpha expression vector. C/EBPalpha transactivated the C7 luciferase reported gene and restored the C7 expression in Hep-G2 cells.