bluuebunny/crossref_metadata_2025_split huggingface dataset:
ASK1–JNK signaling cascade mediates Ad‐ST13‐induced apoptosis in colorectal HCT116 cells
Authors: Yang Min , Yu Mingcan , Guan Dongyin , Gu Jinfa , Cao Xin , Wang Weiyun , Zheng Shu , Xu Yingying , Shen Zonghou , Liu Xinyuan 
Published: April 2010

AbstractST13, a co‐factor of heat shock protein, has shown potential antitumor efficacy for colorectal cancer in our previous study. However, the molecular mechanisms governing ST13‐induced apoptosis are poorly understood. Here, we demonstrate that Ad‐ST13 (ST13 mediated by adenovirus) activates apoptosis signal‐regulated kinase (ASK1) and c‐Jun N‐terminal kinase (JNK) but not p38 (mitogen‐activated protein kinase) in human colorectal HCT116 cells. Ad‐ST13 also increases extracellular‐regulated kinase (ERK) phosphorylation levels, but the change is due to adenovirus replication. Overexpression of ST13 also increases the transcription activity of AP‐1. Blocking ASK1–JNK pathway affects Ad‐ST13‐mediated colorectal cell apoptosis, decreases the release of cytochrome c in cytoplasm and caspase activation. Because ASK1 is known to contain a tetratricopeptide repeat (TPR)‐acceptor site and ST13 has TPR domain, we found the interaction between ST13 and ASK1. These results strongly indicate Ad‐ST13 triggers colorectal cell apoptosis via ASK1–JNK signaling cascade. J. Cell. Biochem. 110: 581–588, 2010. © 2010 Wiley‐Liss, Inc.
Exclusive expression of a membrane‐bound Spink3‐interacting serine protease‐like protein TESPL in mouse testis
Authors: Ou Chung‐Mao , Lin Shih‐Ren , Lin Han‐Jia , Luo Ching‐Wei , Chen Yee‐Hsiung 
Published: April 2010

AbstractWe identified a testis‐specific protease‐like protein tentatively named TESPL and a pancreatic trypsinogen Prss2 from the clones of a yeast two‐hybrid screen against a mouse testicular cDNA library using the trypsin inhibitor Spink3 from male accessory sexual glands as bait. The enzymatic motifs and the cysteine patterns in serine proteases are highly conserved in these two proteins. Based on the phylogenetic analysis, Prss2 duplicated recently and TESPL underwent distant evolution without gene duplication from the progenitor of trypsin‐like and chymotrypsin‐like proteases. We found that TESPL transcription was restricted to the testis and that the level of transcription was positively correlated with animal maturation. In contrast, Prss2 was constitutively expressed in many tissues including testis. Alignment of the cDNA‐deduced sequences of serine proteases showed the replacement of an essential serine residue in the catalytic triad of serine proteases by a proline residue in TESPL, which was demonstrated to be a membrane‐bound protein devoid of proteolytic activity. The immunohistochemical staining patterns of seminiferous tubules in the testis revealed TESPL mainly on postmeiotic cells such as spermatids and spermatozoa. On the mouse sperm from caudal epididymis, TESPL was localized mainly on the plasma membrane overlaying the acrosomal region. Further, orthology group for mouse TESPL was identified in the conserved gene family of eutherian testis serine protease 5. J. Cell. Biochem. 110: 620–629, 2010. © 2010 Wiley‐Liss, Inc.
Tumor necrosis factor alpha induces LIF expression through ERK1/2 activation in mammary epithelial cells
Authors: Levy Carolina Schere , Slomiansky Victoria , Gattelli Albana , Nahmod Karen , Pelisch Federico , Blaustein Matias , Srebrow Anabella , Coso Omar A. , Kordon Edith C. 
Published: April 2010

AbstractIt has been reported that expression of tumor necrosis factor superfamily members occur at the onset of the mammary gland post‐lactational involution. One of these proteins, tumor necrosis factor alpha (TNFα), is a major mediator of inflammation that is able to induce expression of several cytokines. Leukemia inhibitory factor (LIF) is an inflammatory cytokine that is induced and plays a fundamental role during post‐lactational involution of the mammary gland. Therefore, our goal was to determine whether TNFα activity in the mammary epithelium might include regulation of LIF expression. This biological role would increase the significance of TNFα expression at the end of lactation. Our results show that TNFα was able to induce LIF transcription through ERK1/2 activation in a non‐tumorigenic mouse mammary epithelial cell line, SCp2. We found that activation of TNFα receptor‐2 (TNFR2) was specifically involved in triggering this signaling pathway. In addition, our data suggest the participation of AP‐1 transcription factor family members in this pathway. We determined that TNFα treatment induced c‐fos transcription, and blocking AP‐1 activity resulted in a significant inhibition of TNFα‐induced LIF expression. Finally, we found that TNFα was also able to trigger LIF expression and ERK1/2 activation in the mouse mammary gland in vivo. Therefore, our data suggest that TNFα may contribute to mammary gland involution by, among other activities, eliciting LIF expression through ERK1/2 and AP1 activation. J. Cell. Biochem. 110: 857–865, 2010. © 2010 Wiley‐Liss, Inc.
Resveratrol induces cell‐cycle disruption and apoptosis in chemoresistant B16 melanoma
Authors: Gatouillat Grégory , Balasse Emilie , Joseph‐Pietras Débora , Morjani Hamid , Madoulet Claudie 
Published: April 2010

AbstractResveratrol, a naturally occurring polyphenol, has been shown to possess chemopreventive activities. In this study, we show that resveratrol (0–500 µM) inhibits the growth of a doxorubicin‐resistant B16 melanoma cell subline (B16/DOX) (IC50 = 25 µM after 72 h, P < 0.05). This was accomplished by imposing an artificial checkpoint at the G1–S phase transition, as demonstrated by cell‐cycle analysis and down‐regulation of cyclin D1/cdk4 and increased of p53 expression level. The G1‐phase arrest of cell cycle in resveratrol‐treated (10–100 µM) B16/DOX cells was followed by the induction of apoptosis, which was revealed by pyknotic nuclei and fragmented DNA. Resveratrol also potentiated at subtoxic dose (25 µM for 24 h) doxorubicin cytotoxicity in the chemoresistant B16 melanoma (P < 0.01). When administered to mice, resveratrol (12.5 mg/kg) reduced the growth of an established B16/DOX melanoma and prolonged survival (32% compared to untreated mice). All these data support a potential use of resveratrol alone or in combination with other chemotherapeutic agents in the management of chemoresistant tumors. J. Cell. Biochem. 110: 893–902, 2010. © 2010 Wiley‐Liss, Inc.
Runx2/Cbfa1, but not loss of myocardin, is required for smooth muscle cell lineage reprogramming toward osteochondrogenesis
Authors: Speer Mei Y. , Li Xianwu , Hiremath Pranoti G. , Giachelli Cecilia M. 
Published: April 2010

AbstractVascular calcification is a major risk factor for cardiovascular morbidity and mortality. Smooth muscle cells (SMCs) may play an important role in vascular cartilaginous metaplasia and calcification via reprogramming to the osteochondrogenic state. To study whether SM lineage reprogramming and thus matrix calcification is reversible and what the necessary regulatory factors are to reverse this process, we used cells isolated from calcifying arterial medias of 4‐week‐old matrix Gla protein knockout mice (MGP−/−SMCs). We found that vascular cells with an osteochondrogenic phenotype regained SMC properties (positive for SM22α and SM α‐actin) and down‐regulated osteochondrogenic gene expression (Runx2/Cbfa1 and osteopontin) upon culture in medium that favors SMC differentiation. Over time, the MGP−/− SMCs no longer expressed osteochondrogenic proteins and became indistinguishable from wild‐type SMCs. Moreover, phenotypic switch of the restored SMCs to the osteochondrogenic state was re‐induced by the pro‐calcific factor, inorganic phosphate. Finally, loss‐ and gain‐of‐function studies of myocardin, a SM‐specific transcription co‐activator, and Runx2/Cbfa1, an osteochondrogenic transcription factor, revealed that upregulation of Runx2/Cbfa1, but not loss of myocardin, played a critical role in phosphate‐induced SMC lineage reprogramming and calcification. These results are the first to demonstrate reversibility of vascular SMCs in the osteochondrogenic state in response to local environmental cues, and that myocardin‐enforced SMC lineage allocation was not sufficient to block vascular calcification. On the other hand, Runx2/Cbfa1 was found to be a decisive factor identified in the process. J. Cell. Biochem. 110: 935–947, 2010. © 2010 Wiley‐Liss, Inc.
Osteoclast‐specific inactivation of the integrin‐linked kinase (ILK) inhibits bone resorption
Authors: Dossa Tanya , Arabian Alice , Windle Jolene J. , Dedhar Shoukat , Teitelbaum Steven L. , Ross F. Patrick , Roodman G. David , St‐Arnaud René 
Published: April 2010

AbstractBone resorption requires the adhesion of osteoclasts to extracellular matrix (ECM) components, a process mediated by the αvβ3 integrin. Following engagement with the ECM, integrin receptors signal via multiple downstream effectors, including the integrin‐linked kinase (ILK). In order to characterize the physiological role of ILK in bone resorption, we generated mice with an osteoclast‐specific Ilk gene ablation by mating mice with a floxed Ilk allele with TRAP‐Cre transgenic mice. The TRAP‐Cre mice specifically excised floxed alleles in osteoclasts, as revealed by crossing them with the ROSA26R reporter strain. Osteoclast‐specific Ilk mutant mice appeared phenotypically normal, but histomorphometric analysis of the proximal tibia revealed an increase in bone volume and trabecular thickness. Osteoclast‐specific Ilk ablation was associated with an increase in osteoclastogenesis both in vitro and in vivo. However, the mutant osteoclasts displayed a decrease in resorption activity as assessed by reduced pit formation on dentin slices in vitro and decreased serum concentrations of the C‐terminal telopeptide of collagen in vivo. Interestingly, compound heterozygous mice in which one allele of Ilk and one allele of the β3 integrin gene were inactivated (ILK+/−; β) also had increased trabecular thickness, confirming that β3 integrin and Ilk form part of the same genetic cascade. Our results show that ILK is important for the function, but not the differentiation, of osteoclasts. J. Cell. Biochem. 110: 960–967, 2010. © 2010 Wiley‐Liss, Inc.
Valproic acid enhances Oct4 promoter activity in myogenic cells
Authors: Teng Han Fang , Kuo Yu‐Liang , Loo Moo Rung , Li Chung Leung , Chu Ta Wei , Suo Hsien , Liu Hang Seng , Lin Kwang Huei , Chen Shen Liang 
Published: April 2010

AbstractInduced pluripotent stem (iPS) cells are reprogrammed from somatic cells through ectopic expression of stem cell‐specific transcription factors, including Oct4, Nanog, Sox2, Lin28, Klf4, and c‐Myc. Although iPS cells are similar to embryonic stem (ES) cells in their pluripotency, their inherited defects, such as insertion mutagenesis, employment of oncogenes, and low efficiency, associated with the reprogramming procedure have hindered their clinical application. A study has shown that valproic acid (VPA) treatment can significantly enhance the reprogramming efficiency and avoid the usage of oncogenes. To understand how VPA can enhance pluripotency, we stably transfected an Oct4 promoter driven luciferase reporter (Oct4‐1.9k‐Luc) into P19 embryonic carcinoma (EC) cells and C2C12 myoblasts and examined their response to VPA. We found that VPA could both activate Oct4 promoter and rescue its inhibition by retinoic acid (RA). In C2C12 myoblasts, VPA treatment also enhanced endogenous Oct4 expression but repressed that of MyoD. Furthermore, both RARα over‐expression and mutation of a proximal hormone response element (HRE) blocked the activation effect of VPA on Oct4 promoter, implying that VPA may exert its activation effect through factors targeting this HRE. Taken together, these observations identify a molecular mechanism by which VPA directly regulate Oct4 expression to ensure the acquirement and maintenance of pluripotency. J. Cell. Biochem. 110: 995–1004, 2010. © 2010 Wiley‐Liss, Inc.
A comment to the nudged elastic band method
Authors: Quapp Wolfgang , Bofill Josep Maria 
Published: April 2010

AbstractThe minimum energy path (MEP) is an important reaction path concept of theoretical chemistry, and the nudged elastic band (NEB) method with its many facets is a central method to determine the MEP. We demonstrate in this comment that the NEB does not have to lead to a steepest descent pathway (as always assumed). In contrast, as long as it is used without spring forces, it can lead to a gradient extremal. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Adsorption of CO on oxygen preadsorbed neutral and charged gas phase Pd4 clusters: A density functional study
Authors: Kalita Bulumoni , Deka Ramesh C. 
Published: April 2010

AbstractWe present the results of a density functional calculation on adsorption of O2, CO, and their coadsorption at various sites of neutral, cationic, and anionic Pd4 clusters. For all the clusters, the dissociative adsorption of oxygen sitting on Pd bridge sites is found to be preferable. Both O2 and CO binding energies are found to be higher for the anionic Pd4 cluster followed by cationic and neutral cluster. However, binding energies of O2 or CO in the coadsorption complexes follow the trend: anionic > neutral > cationic. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Advanced relationships between categories analysis as a qualitative research tool
Authors: Rabinovich Merav , Kacen Lea 
Published: April 2010

AbstractThe authors propose an advanced relationships between categories (RBC) model as an expansion of Tutty, Rothery, and Grinnell's (1996) qualitative tool for classifying RBC patterns as contained, temporal, and causal relationships. It is assumed that identification of the relationships obtained among categories of qualitative data paves the way for construction of a theory, even though few tools have been developed for this purpose to date. The advanced RBC model points to three additional relationship patterns: bilateral, trilateral, and quadrilateral relationships. These relationships reveal how the text itself links among its various components. The model serves as an innovative tool for systematic derivation of explanations based on the qualitative raw data, contributing to grounded theory and other interpretive studies. © 2010 Wiley Periodicals, Inc. J Clin Psychol: 66:1–11, 2010.
The laminin binding integrin α6β1 in prostate cancer perineural invasion
Authors: Sroka Isis C. , Anderson Todd A. , McDaniel Kathy M. , Nagle Raymond B. , Gretzer Matthew B. , Cress Anne E. 
Published: April 2010

AbstractMetastasizing prostate tumor cells invade along nerves innervating the encapsulated human prostate gland in a process known as perineural invasion. The extacellular matrix laminin class of proteins line the neural route and tumor cells escaping from the gland express the laminin binding integrin α6β1 as a prominent cell surface receptor. Integrin α6β1 promotes aggressive disease and supports prostate tumor cell metastasis to bone. Laminins and their integrin receptors are necessary for the development and maintenance of the peripheral nervous system, indicating the potential role for integrin receptors in directing prostate tumor cell invasion on nerves during perineural invasion. J. Cell. Physiol. 224: 283–288, 2010. © 2010 Wiley‐Liss, Inc.
Estrogen and non‐genomic upregulation of voltage‐gated Na+ channel activity in MDA‐MB‐231 human breast cancer cells: Role in adhesion
Authors: Fraser Scott P. , Ozerlat‐Gunduz Iley , Onkal Rustem , Diss James K.J. , Latchman David S. , Djamgoz Mustafa B.A. 
Published: April 2010

AbstractExternal (but not internal) application of β‐estradiol (E2) increased the current amplitude of voltage‐gated Na+ channels (VGSCs) in MDA‐MB‐231 human breast cancer (BCa) cells. The G‐protein activator GTP‐γ‐S, by itself, also increased the VGSC current whilst the G‐protein inhibitor GDP‐β‐S decreased the effect of E2. Expression of GPR30 (a G‐protein‐coupled estrogen receptor) in MDA‐MB‐231 cells was confirmed by PCR, Western blot and immunocytochemistry. Importantly, G‐1, a specific agonist for GPR30, also increased the VGSC current amplitude in a dose‐dependent manner. Transfection and siRNA‐silencing of GPR30 expression resulted in corresponding changes in GPR30 protein expression but only internally, and the response to E2 was not affected. The protein kinase A inhibitor, PKI, abolished the effect of E2, whilst forskolin, an adenylate cyclase activator, by itself, increased VGSC activity. On the other hand, pre‐incubation of the MDA‐MB‐231 cells with brefeldin A (a trans‐Golgi protein trafficking inhibitor) had no effect on the E2‐induced increase in VGSC amplitude, indicating that such trafficking (‘externalisation’) of VGSC was not involved. Finally, acute application of E2 decreased cell adhesion whilst the specific VGSC blocker tetrodotoxin increased it. Co‐application of E2 and tetrodotoxin inhibited the effect of E2 on cell adhesion, suggesting that the effect of E2 was mainly through VGSC activity. Pre‐treatment of the cells with PKI abolished the effect of E2 on adhesion, consistent with the proposed role of PKA. Potential implications of the E2‐induced non‐genomic upregulation of VGSC activity for BCa progression are discussed. J. Cell. Physiol. 224: 527–539, 2010. © 2010 Wiley‐Liss, Inc.
(p)ppGpp and drug resistance
Authors: Wu Jun , Long Quanxin , Xie Jianping 
Published: April 2010

AbstractIn recent years, emerging and reemerging pathogens resistant to nearly all available antibiotics are on the rise. This limits the availability of effective antibiotics to treat infections, thus it is imperative to develop new drugs. The accumulation of alarmones guanosine tetraphosphate and guanosine pentaphosphate, collectively known as (p)ppGpp, is a global response of bacteria to environmental stress. (p)ppGpp has been documented to be involved in the resistance to β‐lactam and peptide antibiotics. Proposed mechanisms of action include occupation of drug targets, regulation of the expression of virulence determinants, and modification of protein activities. (p)ppGpp analogs might counteract these actions. Several such entities are being tested as new antibiotics. Further insights into the mechanisms of (p)ppGpp‐mediated drug resistance might facilitate the discovery and development of novel antibiotics. J. Cell. Physiol. 224: 300–304, 2010. © 2010 Wiley‐Liss, Inc.
Mechanistic and signaling analysis of Muc4–ErbB2 signaling module: New insights into the mechanism of ligand‐independent ErbB2 activity
Authors: Kozloski Goldi A. , Carraway Coralie A. Carothers , Carraway Kermit L. 
Published: April 2010

AbstractThe membrane mucin Muc4 is aberrantly expressed in numerous epithelial carcinomas and is currently used as a cancer diagnostic and prognostic tool. Muc4 can also potentiate signal transduction by modulating differential ErbB2 phosphorylation in the absence and in the presence of the ErbB3 soluble ligand heregulin (HRG‐β1). These features of Muc4 suggest that Muc4 is not merely a cancer marker, but an oncogenic factor with a unique‐binding/activation relationship with the receptor ErbB2. In the present study, we examined the signaling mechanisms that are associated with the Muc4–ErbB2 module by analyzing ErbB2 differential signaling in response to Muc4 expression. Our study was carried out in the A375 human melanoma and BT‐474 breast cancer cell lines as our model systems. Quantitative and comparative signaling modulations were evaluated by immunoblot using phospho‐specific antibodies, and densitometry analysis. Signaling complex components were identified by chemical cross‐linking, fractionation by gel filtration, immunoprecipitation, and immunoblotting. Activated downstream signaling pathways were analyzed by an antibody microarray screen and immunoblot analyses. Our results indicate that Muc4 modulates ErbB2 signaling potential significantly by stabilizing and directly interacting with the ErbB2–ErbB3 heterodimer. Further analyses indicate that Muc4 promotes ErbB2 autocatalysis, but it has no effect on ErbB3 phosphorylation, although the chemical cross‐linking data indicated that the signaling module is composed of Muc4, ErbB2, and ErbB3. Our microarray analysis indicates that Muc4 expression promotes cell migration by increasing the phosphorylation of the focal adhesion kinase and also through an increase in the levels of β‐catenin. J. Cell. Physiol. 224: 649–657, 2010. © 2010 Wiley‐Liss, Inc.
Immunodeficiency reduces neural stem/progenitor cell apoptosis and enhances neurogenesis in the cerebral cortex after stroke
Authors: Saino Orie , Taguchi Akihiko , Nakagomi Takayuki , Nakano‐Doi Akiko , Kashiwamura Shin‐ichiro , Doe Nobutaka , Nakagomi Nami , Soma Toshihiro , Yoshikawa Hiroo , Stern David M. , Okamura Haruki , Matsuyama Tomohiro 
Published: April 2010

AbstractAcute inflammation in the poststroke period exacerbates neuronal damage and stimulates reparative mechanisms, including neurogenesis. However, only a small fraction of neural stem/progenitor cells survives. In this report, by using a highly reproducible model of cortical infarction in SCID mice, we examined the effects of immunodeficiency on reduction of brain injury, survival of neural stem/progenitor cells, and functional recovery. Subsequently, the contribution of T lymphocytes to neurogenesis was evaluated in mice depleted for each subset of T lymphocyte. SCID mice revealed the reduced apoptosis and enhanced proliferation of neural stem/progenitor cells induced by cerebral cortex after stroke compared with the immunocompetent wild‐type mice. Removal of T lymphocytes, especially the CD4+ T‐cell population, enhanced generation of neural stem/progenitor cells, followed by accelerated functional recovery. In contrast, removal of CD25+ T cells, a cell population including regulatory T lymphocytes, impaired functional recovery through, at least in part, suppression of neurogenesis. Our findings demonstrate a key role of T lymphocytes in regulation of poststroke neurogenesis and indicate a potential novel strategy for cell therapy in repair of the central nervous system. © 2010 Wiley‐Liss, Inc.
Endogenous expression of interleukin‐4 regulates macrophage activation and confines cavity formation after traumatic spinal cord injury
Authors: Lee Seung Ihm , Jeong Soo Ryeong , Kang Young Mi , Han Dae Hee , Jin Byung Kwan , Namgung Uk , Kim Byung G. 
Published: April 2010

AbstractTraumatic spinal cord injury (SCI) triggers inflammatory reactions in which various types of cells and cytokines are involved. Several proinflammatory cytokines are up‐regulated after SCI and play crucial roles in determining the extent of secondary tissue damage. However, relatively little is known about antiinflammatory cytokines and their roles in spinal cord trauma. Recent studies have shown that an antiinflammatory cytokine, interleukin‐4 (IL‐4), is expressed and exerts various modulatory effects in CNS inflammation. We found in the present study that IL‐4 was highly expressed at 24 hr after contusive SCI in rats and declined thereafter, with concurrent up‐regulation of IL‐4 receptor subunit IL‐4α. The majority of IL‐4‐producing cells were myeloperoxidase‐positive neutrophils. Injection of neutralizing antibody against IL‐4 into the contused spinal cord did not significantly affect the expression levels of proinflammatory cytokines such as IL‐1β, IL‐6, and tumor necrosis factor‐α or other antiinflammatory cytokines such as IL‐10 and transforming growth factor‐β. Instead, attenuation of IL‐4 activity led to a marked increase in the extent of ED1‐positive macrophage activation along the rostrocaudal extent at 7 days after injury. The enhanced macrophage activation was preceded by an increase in the level of monocyte chemoattractant protein‐1 (MCP‐1/CCL2). Finally, IL‐4 neutralization resulted in more extensive cavitation at 4 weeks after injury. These results suggest that endogenous expression of antiinflammatory cytokine IL‐4 regulates the extent of acute macrophage activation and confines the ensuing secondary cavity formation after spinal cord trauma. © 2010 Wiley‐Liss, Inc