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PubMed2003

[Mechanisms to control degradation of polyglutamine-containing protein].

Machado-Joseph disease (MJD)/Spinocerebellar ataxia type 3 (SCA3) is neurodegenerative disease which is caused by polyglutamine expansion in a responsible gene product, MJD1/Ataxin3. MJD1 has now been shown to undergo ubiquitylation and degradation by proteasome-dependent pathway. MJD1 with expanded polyglutamine tract was more resistant to degradation than normal MJD1. We established an in vitro system of ubiquitylation of MJD1, thereby biochemically purified activity to mediate polyubiquitylation of MJD1 from rabbit reticulocyte lysate. An AAA-family ATPase VCP was isolated from the active fraction, and found to binds to MJD1. Furthermore, UFD2a, a mammalian ubiquitin-chain assembly factor (E4), associated with VCP and induced polyubiquitylation of MJD1. UFD2a markedly promoted ubiquitylation and degradation of MJD1 with expanded polyglutamine tract, resulting in the clearance of MJD1 protein. In contrast, dominant-negative mutant UFD2a reduced the degradation rate of MJD1, leading to the formation of intracellular aggregation. In Drosophila model, overexpression of UFD2a significantly suppressed the neurodegeneration induced by expression of MJD1 with expanded polyglutamine tract. These findings suggest that E4 is a rate-limiting factor of degradation of pathologic polyglutamine-containing proteins, and may give a potential tool for gene therapy to control the clinical conditions of MJD.

Adenosine Triphosphatases↗

PubMed2004

[Comprehensive prognostic value of spontaneous and evoked electromyography in laryngeal paralysis].

OBJECTIVE: To determine the comprehensive prognostic value of spontaneous and evoked electromyography (EMG) in laryngeal paralysis. METHODS: The characteristics of laryngeal EMG of 91 cases with unilateral vocal cord paralysis (VCP) after thyroid surgery were assessed. All cases were divided into four groups according to the interval of laryngeal EMG after onset, which were group one (2 months shorter, n = 13), group two (2 to 4 months, n = 23), group three (4 to 6 months, n = 36), group four (6 months longer, n = 19). The waveform morphology and the amplitude of laryngeal EMG and the highest evoked compound muscular active potential (CMAP) of thyroarytenoid muscles were examined and analyzed during voluntary tasks. The potential amplitude was showed by the percentage of that of the healthy lateral. The criterion of evaluation on evoked potential was attained by calculating statistical confidence interval. RESULTS: The highest evoked CMAP in group one was significantly lower than that of the others (P < 0.05), but no significant difference was observed between group two and group three (P > 0.05), so group two and group three were analyzed together. There were 2 recovered cases and 11 unrecovered cases in group one. On the basis of this criterion that a positive prognosis for laryngeal recovery was indicated when the evoked CMAP presented and there was no misdirect generated potential, correct prognostic rate was 92% (12/13). There were 11 recovered cases and 48 unrecovered cases in group two and three. The highest evoked CMAP was much higher in the recovered than in the unrecovered, significant difference was observed between them (P < 0.001). On the basis of the criterion that a positive prognosis for laryngeal recovery was indicated when the highest evoked CMAP was higher than 26. 4%, correct prognostic rate was 90% (53/59). On the basis of the criterion that a positive prognosis for laryngeal recovery was indicated when there was no misdirect generated potential and the highest evoked CMAP was higher than 26.4%, correct prognostic rate was 93% (55/59). When the interval from onset to laryngeal EMG recovering was longer than 6 months, none of these patients had return of vocal cord mobility whatever were the outcomes of laryngeal EMG. CONCLUSIONS: Correct prognostic rate can be improved if the prognosis of VCP in different courses is judged respectively by analyzing comprehensively spontaneous and evoked EMG.

Adult↗

PubMed1987

[Body water compartments of patients with chronic heart failure and the refractory edema syndrome].

Using modern methods of investigation body water spaces were studied in 44 persons: 12 healthy ones and 32 patients with various degrees of heart failure. Significant changes in the content and distribution of water with regard to a degree of decompensation were revealed. Dilatation of the volume of extracellular fluid (VEF) was observed in patients with noticeable peripheral edemas as a result of an increase in the volume of circulating plasma (VCP) and an increase in the volume of interstitial fluid (VIF). A considerable increase in the total body water (TBW), VEF and vascular and interstitial portions were noted in the patients with stage IIB-IIIA heart failure in the presence of ascites. The division of the patients into 2 subgroups with relation to the results of subsequent dehydration therapy (22 patients were given diuretic therapy, in the other 10 patients it was supplemented with isolated ultrafiltration due to the refractory edematous syndrome) revealed distinct difference in the basal state of water spaces which manifested itself in a significant increase in VEF and VCP in patients with the refractory edematous syndrome. Thus a study of body water spaces in patients with chronic heart failure was important for the definition of groups of patients with resistance to diuretic therapy. A study of the time course of these parameters under the influence of various dehydration methods is of great interest. A special paper devoted to the problem, will be prepared by the authors.

Adult↗

PubMed1983

[Chemotherapy for advanced non-Hodgkin's lymphoma with CVP therapy].

Thirty-one patients with advanced non-Hodgkin's lymphoma were treated with a combination chemotherapy (VCP therapy), including vincristine (1 mg, weekly), cyclophosphamide (350mg/m2, IV every two weeks) and prednisolone (60mg/day, 1-5 days PO, every two weeks), as an out-patient basis, from May 1974 to October 1977. Characteristics of 31 patients were as follows: median age (56 years), histological types by Rappaport's classification (nodular 2, diffuse 29, NPDL 2, DWDL 5, DPDL 10 and DH 14), clinical stages (II 4, III 9, IV 18), systemic symptoms (A 13, B 18), extranodal presentation (28) and prior treatment (17). Response was evaluated in 28 patients with measurable disease. Complete response (CR) was obtained in 15 patients (53%) and partial response (PR) in 5 (18%). Median time to CR was 20 (6-79) days, and response duration of CR was 14 (1.5-78+) months. Survival time was 19 (1-76) months for all patients, 26 (3-78) months for patients with CR, 9 (3-51) months for patients with PR, and 4 (1-41) months for non-responders. Survival of complete responders was significantly better than that of patients with non-CR. Survival rates of complete responders were 80% (1 year), and 47% (3 year). Toxicities of VCP therapy were relatively mild and reversible with peripheral neuropathy, hair loss and leukopenia. The results indicate that it is necessary to perform more intensive combination chemotherapy adding potent agents for a higher CR rate and a longer CR duration.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1980

Total and regional cerebral blood flow during perfusion from the lateral ventricle to the cisterna magna in the conscious dog: effect of hemorrhagic hypotension and retransfusion on cerebral blood flow.

This study was performed to determine if autoregulation of regional cerebral blood flow (rCBF) occurs in conscious dogs with ventriculocisternal perfusion (VCP) during moderate hypotension. Six dogs were perfused for 360 minutes using mock cerebrospinal fluid (CSF). A 120-minute control period was followed by 180 minutes of moderate hemorrhagic hypotension (mean arterial pressure (SAP) 60-80 mm Hg). The lost blood (approximately 40% of the calculated blood volume) was retransfused after 300 minutes of perfusion, and an additional 60 minutes of observation concluded the study. The rCBF was measured at 120, 240, and 360 minutes of perfusion using labeled microspheres of 15 mu diameter. Cardiac output (CO) was 2.8 +/- 0.41 liters/min at 120 minutes, decreased to 1.4 +/- 0.10 liters/min after hemorrhage, and rose after retransfusion to 2.2 +/- 0.13 liters/min. The percentage of cardiac output (%CO) received by the brain was 1.8 +/- 0.37% at 120 minutes, 3.8 +/- 0.44% at 240 minutes, and 2.2 +/- 0.22% after retransfusion (P < 0.05). There was no significant change in rCBF during hypotension. The regional cerebral blood flow was, however, significantly elevated in the thalamus, mesencephalon, pons, and medulla after retransfusion indicated a local alteration of set point in the plateau of the autoregulatory curve. Cerebral venous pH (measured in internal maxillary venous blood) decreased significantly during hemorrhage to 7.25, while cerebral arteriovenous difference of oxygen and A-VpH increased significantly during hemorrhage. Thus, autoregulation of total cerebral blood flow (CBF) during acute moderate hypotension remains intact during VCP at a rate of 0.2 ml/min using a perfusate of a constant pH and, hence, CSF-pH appears not to be of major significance for the autoregulation of CBF in moderate hypotension.

Animals↗

PubMed1998

Primary Th1 cell immunization against HIVgp160 in SCID-hu mice coengrafted with peripheral blood lymphocytes and skin.

SCID-hu mouse models are of interest in the pathologic investigation of HIV infection, but obtaining a T cell response in SCID-hu-PBL mice is still controversial. We have developed a SCID model by engrafting human skin and autologous PBLs from HIV-seronegative individuals. The study describes the ability of this human-mouse chimera to generate in vivo a primary T lymphocyte response against HIV Ag. The injection of human autologous PBLs was performed 4 to 5 wk after the skin engraftment. Two weeks after injection of PBLs, chimeric mice were immunized with recombinant canary pox virus expressing HIV-1 LAIgp160 (vCP-LAIgp160) and supplemented or not with rIL-2. Intradermal vCP-LAIgp160 injection induced an intradermal perivascular human lymphocytic infiltrate and an epidermic network of CD1a+, CD80+, and CD86+ cells. We derived CD4+ T cell lines (STLs) from the human skin graft of immunized mice, showing that STLs mediated an MHC class II-restricted cytolytic activity directed against HIV-LAIgp160 Ags. Cytokine gene expression in both human skin cells and in STLs showed a predominance of IL-2, IFN-gamma, and IL-12 transcripts. Finally, the T cell repertoire analysis using the immunoscope technique showed a very limited CDR3 length polymorphism in the skin infiltrating lymphocytes suggesting an Ag-specific repertoire. The ability to induce a primary Th1 cell response in vivo affords a useful preclinical model for testing vaccine strategies.

Adoptive Transfer↗

PubMed2006

Manifestations in a family with autosomal dominant bone fragility and limb-girdle myopathy.

We report on an unusual family with an autosomal dominant limb-girdle type of myopathy and bone fragility. This family was previously reported by Henry et al. [1958] as autosomal dominant progressive limb girdle "muscular dystrophy" with propensity to fractures and defective healing of long bones. Clinical, biochemical, and radiological aspects were evaluated in eight living relatives in this family (three males and five females) and in eight deceased individuals. The average age-of-onset of the limb-girdle myopathy was 31 years occurring in 87% of affected individuals. The average age of onset of fractures was 24 years occurring in 88% of affected individuals. Biochemical analysis showed a mean alkaline phosphatase (ALP) of 64 U/L (normal 30-120) and borderline high creatine kinase (CK) of 213 U/L (normal 4-220). Radiographs revealed coarse trabeculation, patchy sclerosis, cortical thickening, and narrowing of the medullary cavity with an appearance not considered typical of Paget disease of bone (PDB) or of fibrous dysplasia. Results of nerve conduction studies were normal, and electromyograms and muscle biopsies documented non-specific myopathic changes. There is premature graying with thin hair, thin skin, hernias and the affected individuals appear older than their chronological age, and three members had a clotting disorder. Linkage analysis for markers for the chromosome 9p22.3-q12 locus indicated that the disorder in this family does not segregate with markers in the critical region of limb-girdle/inclusion body myopathy, PDB, and frontotemporal dementia (FTD) [IBMPFD, OMIM #605382]. Sequencing of Valosin-containing protein (VCP), the gene associated with IBMPFD, did not identify mutations. We have excluded linkage to the known loci for limb-girdle type of myopathy and bone disease and excluded several candidate genes. Elucidation of the novel molecular basis of this disorder may provide valuable links between bone, collagen and muscle, and targeted therapeutic options.

Adult↗

PubMed1993

AFG2, an essential gene in yeast, encodes a new member of the Sec18p, Pas1p, Cdc48p, TBP-1 family of putative ATPases.

A gene from Saccharomyces cerevisiae was sequenced that encodes a protein with homology to a family of putative ATPases. These homologous proteins include the yeast cell division cycle protein Cdc48p and its mammalian homologues VCP and p97; Sec18p and its mammalian homologue NSF, proteins necessary for fusion of transport vesicles to target membranes in the secretory pathway; Pas1p, a protein necessary for peroxisome biosynthesis in yeast; Yme1p, a yeast mitochondrial protein that influences the rate of DNA escape from mitochondria; and TBP-1, MSS1 and Sug1p, proteins that interact with transcription factors. This newly sequenced gene, named AFG2 for ATPase family gene, is located on chromosome XII 5' to the SLP1/VPS33 open reading frame and encodes an essential protein of 780 amino acids that is most homologous to Cdc48p.

Adenosine Triphosphatases↗

PubMed2002

Molecular regulation of muscle cachexia: it may be more than the proteasome.

Muscle cachexia induced by sepsis, severe injury, cancer, and a number of other catabolic conditions is mainly caused by increased protein degradation, in particular breakdown of myofibrillar proteins. Ubiquitin-proteasome-dependent proteolysis is the predominant mechanism of muscle protein loss in these conditions, but there is evidence that several other regulatory mechanisms may be important as well. Some of those mechanisms are reviewed in this article and they include pre-, para-, and postproteasomal mechanisms. Among preproteasomal mechanisms, mediators, receptor binding, signaling pathways, activation of transcription factors, and modification of proteins are important. Several paraproteasomal mechanisms may influence the trafficking of ubiquitinated proteins and their interaction with the proteasome, including the expression and activity of the COP9 signalosome, the carboxy terminus of heat shock protein 70-interacting protein (CHIP) and valosin-containing protein (VCP). Finally, because the proteasome does not degrade proteins completely into free amino acids but into peptides, postproteasomal degradation of peptides by the giant protease tripeptidyl peptidase II (TPP II) and various aminopeptidases is important in muscle catabolism. Thus, multiple mechanisms and regulatory steps may influence the breakdown of ubiquitinated muscle proteins by the 26S proteasome.

Adenosine Triphosphatases↗

PubMed2000

Conserved molecular mechanism for the stage specificity of the mosquito vitellogenic response to ecdysone.

In the mosquito Aedes aegypti, the adult female becomes competent for a vitellogenic response to ecdysone after previtellogenic development. Here, we show that betaFTZ-F1, the nuclear receptor implicated as a competence factor for stage-specific responses to ecdysone during Drosophila metamorphosis, serves a similar function during mosquito vitellogenesis. AaFTZ-F1 is expressed highly in the mosquito fat body during pre- and postvitellogenic periods when ecdysteroid titers are low. The mosquito AaFTZ-F1 transcript nearly disappears in mid-vitellogenesis when ecdysteroid titers are high. An expression peak of HR3, a nuclear receptor implicated in the activation of betaFTZ-F1 in Drosophila, precedes each rise in mosquito FTZ-F1 expression. In in vitro fat body culture, AaFTZ-F1 expression is inhibited by 20-hydroxyecdysone (20E) and superactivated by its withdrawal. Following in vitro AaFTZ-F1 superactivation, a secondary 20E challenge results in superinduction of the early AaE75 gene and the late target VCP gene. Electrophoretic mobility-shift assays show that the onset of ecdysone-response competence in the mosquito fat body is correlated with the appearance of the functional AaFTZ-F1 protein at the end of the previtellogenic development. These findings suggest that a conserved molecular mechanism for controlling stage specificity is reiteratively used during metamorphic and reproductive responses to ecdysone.

Aedes↗

PubMed1977

Combined transtentorial dentatotomy with pulvinarotomy in cerebral palsy.

For frequently associated spasticity with involuntary movements in cerebral palsy operations on cerebellar nuclei or on the pulvinar of the thalamus are recommended. We combined both approaches in 45 patients. The combination was possible after experiences with transtentorial dentatotomy, in which the electrodes are introduced into the deep structures of the cerebellum from a burr-hole on the lambdoid suture. The same lambdoid approach may equally well be applied for introducing electrodes into the pulvinar of the thalamus. The lesion in the pulvinar may moreover be combined with the target in the centrum medianum or in the nuclei VIM-VCP or VOP. Lesions are always asymmetric and multilocular. Their influence on the clinical picture is quite favourable.

Cerebellar Nuclei↗

PubMed2006

Etiologic factors in Paget's disease of bone.

Paget's disease of bone is a chronic focal skeletal disorder characterized by increased bone resorption by the osteoclasts. Paramyxoviral gene products have been detected in pagetic osteoclasts. Paget's disease is an autosomal dominant trait with genetic heterogeneity. Several mutations in the ubiquitin-associated (UBA) domain of sequestosome 1 (SQSTM1/p62) have been identified in patients with Paget's disease. Similarly, mutations in the valosin-containing protein (VCP) gene have been shown to cause inclusion body myopathy associated with Paget's disease of bone and frontotemporal dementia. In addition, gene polymorphisms and enhanced levels of cytokine/growth factors associated with Paget's disease have been identified. However, the etiologic factors in Paget's disease remain elusive. A cause and effect relationship for the paramyxoviral infection and SQSTM1/ p62 gene mutations responsible for pagetic osteoclast development and disease severity are unclear. This article will highlight the etiologic factors involved in the pathogenesis of Paget's disease.

Adaptor Proteins, Signal Transducing↗

PubMed1999

[Preoperative changes in fluid filtration capacity in patients undergoing vascular surgery].

UNLABELLED: Patients undergoing major vascular surgery frequently require a substantial intraoperative fluid replacement to assure hemodynamic stability, which is in excess of the expected fluid requirements due to starving, blood and insensible losses. This leads to a positive fluid balance which can not be readily explained. METHOD: We have used venous congestion plethysmography (VCP) a non-invasive method for measurement of microvascular parameters in limbs to investigate the changes in microvascular permeability (FFK) and the balance of Starling forces of patients undergoing surgery for unilateral femoral artery reconstruction (FEM) under epidural anaesthesia or abdominal aortic aneurysm repair (AAA) under general anaesthesia. The control group consisted of patients scheduled for inguinal hernia repair or hand surgery under general anaesthesia. All patients were measured 24 hours pre-operatively, immediately after the induction of anaesthesia or completion of epidural anaesthesia and on the 1st, 5th and 10th postoperative day. The perioperative patient management followed a standard protocol and all patients with vascular disease were invasively monitored using indwelling arterial lines and central venous catheters. Continuous infusion of Ringers lactate and 6% Dextran 60 was sustained during the induction period. Each patient gave informed consent. RESULTS: Preoperatively we found no significant difference in the mean FFK-values of controls (4.1 +/- 0.4, ml.min-1 100 ml tissue-1 mmHg-1 x 10(-3) = FFKU), the AAA (3.6 +/- 0.3 FFKU) and FEM (4.2 +/- 0.3 FFKU). After induction of anaesthesia the mean FFK value in the controls fell to 3.5 +/- 0.5 FFKU (p = 0.07), whereas in the AAA patients we observed a significant increase to 4.7 +/- 0.2 FFKU (p < 0.005) and after epidural anaesthesia in FEM to 5.5 +/- 0.4 FFKU (p < 0.001) respectively. Those post anaesthetic FFK values where significantly higher in FEM and AAA than in the controls (p < 0.02). In AAA we found a significant positive correlation between the increase in FFK and the intraoperative fluid balance (r2 = 0.69, p < 0.01). No such correlation was found in controls and FEM. The postoperative values of FFK where unchanged in the control group, whereas a further increase was seen in both patient groups with vascular disease, with a maximum in AAA on the 1st postoperative day (to 5.4 +/- 0.4 FFKU mean both legs) and the 5th postoperative day in FEM (to 7.3 +/- 1.7 non-ischemic leg, 7.1 +/- 1.2 ischemic leg FFKU). In both groups normal FFK values where found on the 10th day after the operation. CONCLUSION: The data presented suggests an increase in extravascular fluid loss in patients undergoing vascular surgery, which becomes evident after the induction of general anaesthesia or completion of epidural anaesthesia. The positive correlation with the intraoperative fluid requirements may partially explain the often reported large intraoperative fluid requirements of patients undergoing AAA repair. The fact that the maximum change in fluid filtration capacity is found postoperatively may be explained by the additional effect of an ischemia/reperfusion injury in response to both the clamping an declamping of the artery and the increase in arterial blood flow to the limb due to the successful reconstruction of the blood vessel.

Adult↗

PubMed2001

Post-intubation vocal cord paralysis: the viral hypothesis. A case report.

After digestive surgery, a 20-year-old man presented dysphonia and fever. Indirect laryngoscopy revealed a left vocal cord paralysis with no structural lesion. IgM and IgG were positive for cytomegalovirus and negative for human immunodeficiency virus, herpes simplex virus, varicella zoster virus and Epstein-Barr virus. The patient recovered spontaneously with a normal voice, and the mobility of vocal cord recovered within 3 months. The aetiology of post-intubation vocal cord paralysis (VCP) remains controversial. Vocal cord paralysis with cytomegalovirus has been reported in two cases associated with acquired immunodeficiency syndrome. Vocal cord paralysis secondary to viral disease has also been described in other circumstances. panied by polyneuritis, especially in immunocompromised patients. We report the case of a patient with transitory unilateral post-intubation vocal cord paralysis which could have been related to a virus infection.

Adult↗

PubMed2006

Genetic prognostic index influences patient outcome for node-positive breast cancer.

PURPOSE: To establish a novel genetic prognostic index among node-positive breast cancer patients. METHODS: Using a cDNA microarray, the gene expression profiles of 20 primary breast cancers that had metastasis to four or more axillary lymph nodes were examined. Ten patients survived disease-free for more than 5 years (5S), while ten patients died of breast cancer within 5 years of surgery (5D). RESULTS: A set of genes characterizing each group was identified. Sixteen genes were underexpressed in 5D compared to 5S, and 15 genes were underexpressed in 5S in comparison to 5D. The prognostic index (PI) was established, which could predict the postoperative outcome with five genes that were commonly underexpressed in the 5D group; these genes encoded granulin (GRN), heat shock 90 kDa protein 1 beta (HSPCB), large tumor suppressor homolog 1 (LATS1), valosin-containing protein (VCP), and LIM-and-SH3 protein1 (LASP1). CONCLUSION: These five genes might play an important role in deciding the behavior of node-positive breast cancer. The PI system could thus predict the prognosis of node-positive breast cancer, and might therefore be able to provide valuable information for the prognosis of breast cancer patients.

Adult↗

PubMed1991

PAS1, a yeast gene required for peroxisome biogenesis, encodes a member of a novel family of putative ATPases.

PAS genes are required for peroxisome biogenesis in the yeast S. cerevisiae. Here we describe the cloning, sequencing, and characterization of the PAS1 gene. Its gene product, Pas1p, has been identified as a rather hydrophilic 117 kd polypeptide. The predicted Pas1p sequence contains two putative ATP-binding sites and reveals a structural relationship to three other groups of proteins associated with different biological processes such as vesicle-mediated protein transport (NSF and Sec18p), control of cell cycle (Cdc48p, VCP, and p97-ATPase), and modulation of gene expression of the human immunodeficiency virus (TBP-1). The proteins share a highly conserved domain of about 185 amino acids including a consensus sequence for ATP binding. We suggest that these proteins are members of a novel family of putative ATPases and may be descendants of one common ancestor.

Adenosine Triphosphatases↗

PubMed2005

Proteomic identification of proteins conjugated to ISG15 in mouse and human cells.

Though the interferon-inducible protein ISG15 was one of the first ubiquitin-like modifiers to be discovered, much remains unknown about the identity of proteins conjugated to ISG15 or the biologic consequences of modification. To gain a better understanding of the cellular pathways affected by ISG15, we identified proteins targeted for ISGylation using a proteomic approach. Mass spectrometric analysis identified 76 candidate ISGylation targets in anti-ISG15 immunoprecipitates from interferon-treated mouse or human cells. Twenty-one proteins were found in both mouse and human samples, including STAT1, a known target of ISGylation. Candidates identified in both species were tested for ISGylation in a transfection system: 18 of 19 proteins tested were ISGylated in this system. Two candidates, EF-2 and VCP, were also shown to be ISGylated in an interferon-dependent manner in the absence of exogenous over-expression. Seven proteins identified from a single species, but functionally related to candidates found in both species, were also ISGylated in the over-expression system. Proteins that can be ISGylated play important roles in translation, glycolysis, stress responses, and cell motility. These data indicate that ISGylation targets proteins found in several fundamentally important cellular pathways and will contribute to understanding the physiologic role of interferon-induced ISG15 and ISG15 conjugation.

Animals↗

PubMed2006

Cloning and characterisation of two natural killer enhancing factor genes (NKEF-A and NKEF-B) in pufferfish, Tetraodon nigroviridis.

Natural killer cell enhancing factor (NKEF) belongs to a highly conserved peroxiredoxin (Prx) family. Its functions are involved in immune cytotoxicity, apoptosis, cell proliferation, differentiation and antioxidant activity. In present paper, two NKEF genes, NKEF-A and NKEF-B, were isolated and characterised in spotted green pufferfish, Tetraodon nigroviridis. Comparative genomic location analysis shows conserved syntenies within the NKEF-A and NKEF-B regions between Tetraodon and human, indicating that the Tetraodon NKEF-A and NKEF-B genes are orthologs for mammalian NKEF-A and NKEF-B encoding genes, respectively. The genomic organisation of the two genes is similar in different species, containing one non-coding exon, five coding exons and five introns. The deduced amino acids of the two genes are highly homologous with mammalian NKEF-A and NKEF-B proteins, including two well conserved Val-Cys-Pro (VCP) motifs. Tissue specific expression analysis by RT-PCR reveals that both genes are globally expressed. Stimulation with LPS inhibits both NKEF-A and NKEF-B gene expression in most tissues but enhances NKEF-A and NKEF-B transcriptions in spleen. This is the first report on the existence of a NKEF-B homologue in fish.

Amino Acid Sequence↗