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IL-6 signaling plays a crucial role in the survival and metastasis of skin cancer. NEDD4L acts as a suppressor of IL-6 signaling by targeting GP130 degradation. However, the effects of the NEDD4L-regulated IL-6/GP130 signaling pathway on skin cancer remain unclear. In this study, protein expression levels of NEDD4L and GP130 were measured in tumor tissues from patients with cutaneous squamous cell carcinoma. Skin tumors were induced in wild-type and Nedd4l-knockout mice, and activation of the IL-6/GP130/signal transducer and activator of transcription 3 signaling pathway was detected. The results indicated a negative correlation between the protein expression levels of NEDD4L and GP130 in cutaneous squamous cell carcinoma tissues from patients. Nedd4l deficiency significantly promoted 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-acetate-induced skin tumorigenesis and benign-to-malignant conversion by activating the IL-6/GP130/signal transducer and activator of transcription 3 signaling pathway, which was abrogated by supplementation with the GP130 inhibitor SC144. Furthermore, our findings suggested that NEDD4L can interact with GP130 and promote its ubiquitination in skin tumors. In conclusion, our results indicate that NEDD4L could act as a tumor suppressor in skin cancer, and inhibition of GP130 could be a potential therapeutic method for treating this disease., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Metagenomic next-generation sequencing (mNGS) is valuable for pathogen identification; however, distinguishing between infectious diseases and conditions with potentially similar clinical manifestations, including malignant tumors, is challenging. Therefore, we developed a method for simultaneous detection of infectious pathogens and cancer in blood samples., Methods: Plasma samples (n = 244) were collected from 150 and 94 patients with infections and hematological malignancies, respectively, and analyzed by mNGS for pathogen detection, alongside human tumor chromosomal copy number variation (CNV) analysis (≥5Mbp or 10Mbp CNV region). Further, an evaluation set, comprising 87 plasma samples, was analyzed by mNGS and human CNV analysis, to validate the feasibility of the method., Results: Among 94 patients with hematological malignancy, sensitivity values of CNV detection for tumor diagnosis were 69.15 % and 32.98 % for CNV region 5Mbp and 10Mbp, respectively, with corresponding specificities of 92.62 % and 100 % in the infection group. Area under the ROC curve (AUC) values for 5Mbp and 10Mbp region were 0.825 and 0.665, respectively, which was a significant difference of 0.160 (95 % CI: 0.110-0.210; p < 0.001), highlighting the superiority of 5Mbp output region data. Six patients with high-risk CNV results were identified in the validation study: three with history of tumor treatment, two eventually newly-diagnosed with hematological malignancies, and one with indeterminate final diagnosis., Conclusions: Concurrent CNV analysis alongside mNGS for infection diagnosis is promising for detecting malignant tumors. We recommend adopting a CNV region of 10Mbp over 5Mbp for our model, because of the lower false-positive rate (FPR)., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

The human induced pluripotent stem cell (iPSC) line SMBCi017-A was derived from urine cells of a 20 year old male healthy control donor. The generated iPSCs had normal karyotype, expressed chromosomal stability pluripotency hallmarks and differentiated into the three primary germ layers., (Copyright © 2022. Published by Elsevier B.V.)

Congenital talipes equinovarus (CTEV) is a congenital malformation affecting approximately 1/700-1/1000 of live borns. To date extensive epidemiological and biological studies have been operated to solve this issue, the most meaningful findings in clubfoot genetics involve PITX1 variants, which were associated with clubfoot phenotype in mice and humans. According to recent studies, the PITX1-TBX4 transcriptional pathway regulatory for early limb development has identified a key developmental pathway in clubfoot etiology by the common disease-rare hypothesis. However, the precise mechanisms causing this disease remain elusive. The pluripotent stem cell line SMBCi018-A will enable proper in vitro disease modeling of CTEV., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Methylmalonic acidemia(MMA) is an autosomal recessive hereditary disease caused by methylmalonyl-CoA mutase defect or its coenzyme cobalamin metabolism defect. The mutation of the MMACHC gene leads to metabolic disorder of coenzyme cobalamin, resulting in abnormal accumulation of methylmalonic acid, and finally leads to impairment of multiple organs' functions. Here we generated an induced pluripotent stem cells (iPSCs) line named SMBCi019-A, using urine cells (UCs) derived from a 10-year-old male MMA patient who carried two heterozygous gene mutations in MMACHC c.438G > A (p.w146x) and c.609G > A (p.w203x). The generated iPSCs retained the mutations can function as a cellular model of MMA., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Osteogenesis imperfecta (OI) is a group of genetic disorders characterized mainly by fractures and bone deformities. It has been established that gene mutations, particularly those in COL1A1 and COL1A2, account for most phenotypes. Here, we generated an induced pluripotent stem cells (iPSCs) line named SMBCi014-A using urine cells (UCs) derived from a 15-year-old female OI type I patient who carried the frame-shift mutation of the COL1A1 gene (exon35:c.2450delC:p.P817fs). The patient had a family history of mild fractures and a blue sclera. Therefore, our study established a patient-derived site-specific cellular model of OI to better understand the osteogenic mechanism., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Prader-Willi syndrome (PWS) is a neurodevelopmental disorder caused by deficiency of paternal gene expression in the 15q11.2-q13 chromosome imprinted region. Hyperphagia and dysgnosia are typical clinical features in the early-childhood of patient. We generated an induced pluripotent stem cell (iPSC) line SMBCi011-A from a 6 years old male PWS patient, the line expressed pluripotent signs and had ability to differentiate into three germ layers in vivo., (Copyright © 2022. Published by Elsevier B.V.)

Familial hypercholesterolemia (FH; OMIM: # 143890) is a common inherited autosomal dominant disease, characterized by high-level low-density lipoprotein cholesterol (LDL-C) in plasma. Elevated LDL-C levels is closely related with atherosclerotic plaques and premature cardiovascular disease if not treated in time. Here we generated an induced pluripotent stem cell (iPSC) line using urine cells (UCs) derived from an 8-year-old male FH patient who carrying two coding and pathogenic mutations of low-density lipoprotein receptor (LDLR) gene (exon12:c.C1747T and exon13: c. 1948 del G). This induced pluripotent stem cell line named SMBCi009-A can be used to understand more cellular details about FH., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021. Published by Elsevier B.V.)

The human induced pluripotent stem cell (iPSC) line SMBCi013-A was derived from urine cells of a 29 year old male affected by Wilson's disease. Two heterozygous mutations in the ATP7B gene were detected by whole exon sequencing (c.2303C > A and c.3334C > T). The reprogramming factors (OCT-4, SOX-2, KLF4, miR-302-367) were delivered using non-integrating episomal plasmids. The resulting iPSCs were pluripotent, have chromosomal stability, and the ability to differentiate into the three germ layers., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Multiple Osteochondroma is an abnormal skeleton development autosomal dominant genetic disease which caused by the mutation of EXT1 gene. In this study, we generated induced pluripotent stem cells (iPSCs) from the mesenchymal stem cells (MSCs) of a 12-year-old male patient by reprogramming MSCs with non-integrative vectors. The iPSCs line expresses pluripotent markers, has a normal male karyotype and can differentiate into the three germ layers., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

A non-integrated induced pluripotent stem cell (iPSC) line was established using urine cells (UCs) derived from a healthy 32-year-old male. The patient-derived iPSC line SMBCi006-A exhibited a normal karyotype, expressed pluripotency markers and possessed trilineage differentiation potential. This cell line may serve as a basis for disease modeling, and help explore the molecular pathogenesis further., (Copyright © 2020. Published by Elsevier B.V.)

A human induced pluripotent stem cell (iPSC) line was generated from the urine cells of a 8-year-old female with Gaucher disease with the homozygous changes c.1448 T>C in the GBA gene. Reprogramming factors OCT4, SOX2, KLF4, and miR-302-367 were delivered using a non-integrative plasmid. Our iPSCs showed complete pluripotency, normal genetic stability, and the ability to differentiate into three germ layers., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020. Published by Elsevier B.V.)

Mutations in the neurofibromin (NF1) gene cause neurofibromatosis type 1 (NF1), a complex tumour predisposition syndrome. Here, we generated two induced pluripotent stem cell (iPSC) lines using urine cells (UCs) derived from a 21-year-old female NF1 patient carrying c.496&#95;497delGT mutation in the NF1 gene (p.Val166LeufsTer7). The newly derived SMBCi003-A and SMBCi003-B iPSC lines used as a cellular model to unravel pathogenesis of NF1., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Alzheimer's disease (AD) is a serious neurodegenerative disease. Senile plaques (SPs) in the extracellular space and neurofibrillary tangles (NFTs) in the intracellular areas of the brain are two typical features of AD. SPs and NFTs are composed of amyloid-β (Aβ) aggregates and hyperphosphorylated Tau, respectively. (m)RVD-hemopressin (RVD), which is derived from mouse brain peptide, binds to the cannabinoid 1 receptor (CB1R) as an agonist. Our previous study indicated that RVD reversed Aβ1-42-induced memory impairment in mice. Here, we investigated the underlying molecular mechanism of RVD on Aβ1-42-induced neurotoxicity in retinoic acid-differentiated human neuroblastoma SH-SY5Y cells. Cell viability and neurite outgrowth were investigated by live cell imaging and analysis instrument. We found that RVD reversed Aβ1-42-induced Tau phosphorylation, apoptosis and suppression of neurite outgrowth and the synapse-associated protein postsynaptic density protein 95 (PSD-95) by inhibiting the activity of protein kinase A (PKA) and glycogen synthase kinase 3β (GSK-3β). Combined treatment with AM251 (a CB1R antagonist) blocked the effects of RVD. In conclusion, RVD may be a potential therapeutic agent for the treatment of cognitive dysfunctions, such as Alzheimer's disease., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

A human induced pluripotent stem cell (iPSC) line (SMBCi002-A) was established from amniocytes (amniotic fluid cells, AFDCs) from a 16-week-old female fetus with clubfoot. Reprogramming and enhancing factors OCT4, SOX2, KLF4, MYC, LIN28 and EBNA1 were delivered using a nonintegrative strategy based on episomal plasmids. Validation assays indicated that this iPSC line has full pluripotency, differentiation potential and genetic stability. Currently, the etiology and mechanism of clubfoot remain unclear; therefore, this in vitro cellular model would provide a useful resource for understanding the pathology of this disease., Competing Interests: Declaration of Competing Interest We confirm that the manuscript has been read and approved by all named authors and that there are no other persons who satisfied the criteria for authorship but are not listed. We further confirm that the order of authors listed in the manuscript has been approved by all of us. We confirm that we have given due consideration to the protection of intellectual property associated with this work and that there are no impediments to publication, including the timing of publication, with respect to intellectual property. In so doing we confirm that we have followed the regulations of our institutions concerning intellectual property., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

The microRNA (miRNA) locus miR-144/451 is abundantly expressed in erythrocyte precursors, facilitating their terminal maturation and protecting against oxidant stress. However, the full repertoire of erythroid miR-144/451 target messenger RNAs (mRNAs) and associated cellular pathways is unknown. In general, the numbers of mRNAs predicted to be targeted by an miRNA vary greatly from hundreds to thousands, and are dependent on experimental approaches. To comprehensively and accurately identify erythroid miR-144/451 target mRNAs, we compared gene knockout and wild-type fetal liver erythroblasts by RNA sequencing, quantitative proteomics, and RNA immunoprecipitation of Argonaute (Ago), a component of the RNA-induced silencing complex that binds miRNAs complexed to their target mRNAs. Argonaute bound ∼1400 erythroblast mRNAs in a miR-144/451-dependent manner, accounting for one-third of all Ago-bound mRNAs. However, only ∼100 mRNAs were stabilized after miR-144/451 loss. Thus, miR-144 and miR-451 deregulate <10% of mRNAs that they bind, a characteristic that likely applies generally to other miRNAs. Using stringent selection criteria, we identified 53 novel miR-144/451 target mRNAs. One of these, Cox10 , facilitates the assembly of mitochondrial electron transport complex IV. Loss of miR-144/451 caused increased Cox10 mRNA and protein, accumulation of complex IV, and increased mitochondrial membrane potential with no change in mitochondrial mass. Thus, miR-144/451 represses mitochondrial respiration during erythropoiesis by inhibiting the production of Cox10., (© 2019 by The American Society of Hematology.)

Wilson's disease (WD) is a rare autosomal recessive disorder of copper metabolism caused by an ATP7B gene mutation. Except for hepatic, neurological symptoms, lower bone mineral density is another most frequent clinical features of WD, but the underlying mechanisms have not been fully understood. This article aims to use induced pluripotent stem cells (iPSCs) to establish cellular osteoblasts model related to WD to identify abnormal osteogenesis and signaling pathways. In this study, we successfully produced functional osteoblasts from normal and WD iPSCs through embryoid bodies (EBs) formation method, and then we found WD osteoblasts may have a lower osteogenesis activity than normal controls by detection of osteogenic marker genes and mineralization ability. Further, through gene expression profiling, detection of β-catenin in total protein and nuclear protein, and the nuclear localization of β-catenin, we identified and validated that low osteogenic activity in WD may be due to abnormal β-catenin pathway. Interestingly, we found SKL2001, a small molecule can reverse decreased osteogenesis of WD. In summery, our results suggested that the low bone density of WD may caused by abnormal β-catenin signaling pathway, and these may provided a new target for the treatment of WD., (Copyright © 2019. Published by Elsevier Inc.)

Background: A few studies have evaluated the expression of chemokine receptors CXCR4 and CCR7 in diffuse large B-cell lymphoma (DLBCL); however, the association between CXCR4 and CCR7 with bone marrow (BM) involvement and their synergistic effect on prognosis is still unclear. Our study investigated this aspect., Methods: Specimens were obtained from 61 primary nodal DLBCL patients and 100 reactive proliferative lymphadenitis patients. CXCR4 and CCR7 expression levels were examined by immunohistochemical staining; the relationship between these levels and clinical parameters and the differences in overall survival were analyzed., Results: CXCR4 and CCR7 overexpression was observed in the malignant lymph node tissues from most DLBCL patients. CCR7 expression was significantly higher in the non-GCB than the GCB subtype; CXCR4 positivity rates showed no significant difference between the 2 subtypes. In DLBCL patients with BM involvement, CXCR4 was overexpressed in almost all BM samples, but CCR7 expression was low in BM. CXCR4 overexpression was associated with advanced Ann Arbor stages, MYC overexpression, and increased extranodal infiltration; CCR7 was associated with advanced Ann Arbor stages and elevated LDH. Like the case for CCR7, the survival rate of CXCR4-positive DLBCL patients was significantly lower than that of the CXCR4-negative patients. CXCR4 + CCR7 + patients had the lowest survival rate., Conclusions: There is a positive correlation between CXCR4 overexpression and BM involvement. CXCR4 and CCR7 overexpression is associated with poorer overall survival, especially in CXCR4 and CCR7 copositive patients. CXCR4, CCR7, Ki-67 index, and MYC were independent prognostic factors for DLBCL. Blocking CXCR4 and/or CCR7 can be a novel therapeutic strategy for DLBCL., (Copyright © 2019. Published by Elsevier Inc.)

Many regulators have been identified to participate in the cross-talk between muscle and bone, however, most previous studies focus on secreting proteins. In this study, we demonstrated that exosomes from myoblasts C2C12 can promote pre-osteoblasts MC3T3-E1 differentiation to osteoblasts. We revealed that the effect of C2C12 exosomes depended on its miR-27a-3p component, they can increase miR-27a-3p level in the recipient cells, and decrease its direct target adenomatous polyposis coli (APC) expression, thus activating β-catenin pathway. Furthermore, C2C12 exosomes failed to exert above effects when miR-27a-3p was deprived. These findings indicates exosomal microRNAs can be regarded as a novel type of "myokines" with osteogenesis promoting potential, which would broad our understanding of the muscle-bone interaction under physiological and pathological conditions., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a collagen-binding proteoglycan highly expressed in the developing bones. Recent studies indicated that PRELP could inhibit osteoclastogenesis as a NF-κB inhibitor. However, its role during osteoblast differentiation is still unclear. In this study, we confirmed that the expression of PRELP increased with the osteogenesis induction of preosteoblastic MC3T3-E1 cells. Down-regulation of PRELP expression by shRNA reduced ALP activity, mineralization and expression of osteogenic marker gene Runx2. Our microarray analysis data suggested that β-catenin may act as a hub gene in the PRELP-mediated gene network. We validated furtherly that PRELP knockdown could inhibit the level of connexin43, a key regulator of osteoblast differentiation by affecting β-catenin protein expression, and its nuclear translocation in MC3T3-E1 preosteoblasts. Therefore, this study established a new role of PRELP in modulating β-catenin/connexin43 pathway and osteoblast differentiation., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: This study investigated the status of isolated superior mesenteric artery (SMA) dissection in the most populous country, China., Methods: The Chinese-language literature published before December 2014 was reviewed. All case reports and series were included. If multiple reports originated from the same hospital and included overlapping time frames, only the most recent report was included. The clinical characteristics, imaging features, and treatment were analyzed. "Symptom relief" was used as the outcome measure., Results: A total of 622 patients (88.5% male) with isolated SMA dissection were found in the Chinese-language literature. Patients were a mean age of 55.4 years. Analysis of the demographic data showed that isolated SMA dissection was most reported from the developed areas of China. The most common symptom (91.1%) was abdominal pain, and 42.7% patients had hypertension as a complication. Contrast-enhanced computed tomography was used to diagnose 95.2% of patients. The mean distance from the SMA ostium to the beginning of the dissection was 20.1 mm (range, 0-65.0 mm). The mean length of dissection was 63.1 mm (range, 10.7-205.9 mm). The percentages of patients who underwent primary conservative, surgical, and endovascular treatments were 63.2%, 3.2% and 33.6%, respectively. As primary management, the symptom relief rate of conservative management, with or without anticoagulation, was 62.6% and 86.5%, respectively. The best result of conservative treatment was achieved in cases of Yun type I and Luan classification type B. The symptom relief rate of surgical and endovascular treatment was 100% and 95.2%, respectively., Conclusions: The incidence of isolated SMA dissection may not be as rare as previously reported. Endovascular treatment of isolated SMA dissection is commonly used in China as a first-line treatment., (Copyright © 2016 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

Mammals express thousands of long noncoding (lnc) RNAs, a few of which are known to function in tissue development. However, the entire repertoire of lncRNAs in most tissues and species is not defined. Indeed, most lncRNAs are not conserved, raising questions about function. We used RNA sequencing to identify 1109 polyadenylated lncRNAs expressed in erythroblasts, megakaryocytes, and megakaryocyte-erythroid precursors of mice, and 594 in erythroblasts of humans. More than half of these lncRNAs were unannotated, emphasizing the opportunity for new discovery through studies of specialized cell types. Analysis of the mouse erythro-megakaryocytic polyadenylated lncRNA transcriptome indicates that ~75% arise from promoters and 25% from enhancers, many of which are regulated by key transcription factors including GATA1 and TAL1. Erythroid lncRNA expression is largely conserved among 8 different mouse strains, yet only 15% of mouse lncRNAs are expressed in humans and vice versa, reflecting dramatic species-specificity. RNA interference assays of 21 abundant erythroid-specific murine lncRNAs in primary mouse erythroid precursors identified 7 whose knockdown inhibited terminal erythroid maturation. At least 6 of these 7 functional lncRNAs have no detectable expression in human erythroblasts, suggesting that lack of conservation between mammalian species does not predict lack of function.

Objective: We report our experience in the treatment of isolated superior mesenteric artery dissection and review the clinical and imaging features reported in the literature., Methods: A retrospective study was conducted of 18 consecutive patients with isolated superior mesenteric artery dissection who presented at the Peking University Third Hospital between September 2008 and May 2012. Their clinical characteristics, including age, sex, medical history, risk factors, symptoms, diagnostic imaging modality, and treatment, were analyzed. Also reviewed were 278 patients with isolated superior mesenteric artery dissection reported in the English language literature. The epidemiology, mechanism, clinical presentation, imaging features, and treatment were discussed., Results: There were 14 men and four women with a mean age of 55.6 years (range, 41-84 years). Four patients were asymptomatic, and 14 presented with acute-onset abdominal pain. The diagnosis was established by contrast-enhanced computed tomography in 17 patients and ultrasound imaging in one patient. All dissections were located at the anterior wall and around the convex curvature of the superior mesenteric artery. The decision to intervene was based on symptoms. Three asymptomatic patients underwent successful conservative management, and one asymptomatic patient with an aneurysmal dilated false lumen underwent endovascular stent placement. For the 14 symptomatic patients, definitive treatment included catheter-directed infusion of a vasodilator in four and stent placement combined with catheter-directed infusion of a vasodilator in 10, of whom one patient underwent hybrid stent placement. No complications or deaths occurred. During the mean 14.9-month (range, 1-40 month) follow-up period, all patients were asymptomatic, and patency of the superior mesenteric artery was demonstrated by contrast-enhanced computed tomography scan., Conclusions: Conservative management can be applied to asymptomatic patients with isolated superior mesenteric artery dissection. For symptomatic patients, stent placement is the definitive treatment if there is no arterial rupture or intestinal necrosis. Self-expanding bare stents that completely cover the curvature of the superior mesenteric artery are recommended. Catheter-directed infusion of a vasodilator can be an effective accessional process after stent placement., (Copyright © 2013 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

Glutathione-S-transferases have been identified in all the living species examined so far, yet little is known to date about them in amphioxus, a model organism for insights into the origin and evolution of vertebrates. We have isolated a cDNA encoding an amphioxus (Branchiostoma belcheri) glutathione-S-transferase with a predicted molecular mass of approximately 26 kDa, from the gut cDNA library. The glutathione-S-transferase had 43.7-51.8% identity to most glutathione-S-transferases identified from aquatic organisms including fish and green alga, but it was much less identical (<27%) to other cytosolic glutathione-S-transferase classes. The phylogenetic analysis revealed that the glutathione-S-transferase was grouped together with most piscine and algal glutathione-S-transferases, separating from other cytosolic glutathione-S-transferase classes. Moreover, the glutathione-S-transferase had an exon-intron organization typical of zebrafish putative GST, red sea bream GSTR1 and plaice GSTA1 genes. The recombinant glutathione-S-transferase has been successfully expressed and purified, which showed a relatively high catalytic activity (3.37+/-0.1 unit/mg) toward 1-chloro-2, 4-dinitrobenzene and a moderate activity toward ethacrynic acid (0.41+/-0.01 unit/mg), although it had no detectable activity toward 1, 2-dichloro-4-nitrobenzene, 4-hydroxynonenal, 4-nitrobenzyl chloride and cumene hydroperoxide. In addition, we have revealed a tissue-specific expression pattern of the glutathione-S-transferase gene in B. belcheri, with the most abundant expression in the hepatic caecum. All these indicate that the amphioxus glutathione-S-transferase belongs to a novel rho-class of glutathione-S-transferases with a tissue-specific expression pattern. The relation between the glutathione-S-transferase expression in amphioxus hepatic caecum and the origin of vertebrate liver is also discussed.