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Nigerian Journal of Physiological Sciences     Open Access  
NJAS - Wageningen Journal of Life Sciences     Full-text available via subscription   (Followers: 1)
NMR in Biomedicine     Hybrid Journal   (Followers: 1)
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  First | 6 7 8 9 10 11 12 13 | Last

Journal Cover Biochemistry and Cell Biology
   [10 followers]  Follow    
   Full-text available via subscription Subscription journal
     ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
     Published by NRC Research Press Homepage  [18 journals]   [SJR: 1.488]   [H-I: 65]
  • Involvement of ERK1/2, p38 MAPK, and PI3K/Akt signaling pathways in the
           regulation of cell cycle progression by PTHrP in colon adenocarcinoma
    • Authors: Natalia Calvo; María Julia Martín, Ana Russo de Boland, Claudia Gentili
      Abstract: Biochemistry and Cell Biology, e-First Articles. Parathyroid hormone-related peptide (PTHrP) is distributed in most fetal and adult tissues, and its expression correlates with the severity of colon carcinoma. Recently we obtained evidence that in Caco-2 cells, a cell line from human colorectal adenocarcinoma, exogenous PTHrP increases the number of live cells, via ERK1/2, p38 MAPK, and PI3-kinase and induces the expression of cyclin D1, a cell cycle regulatory protein. In this study, we further investigated the role of PTHrP in the regulation of the cell cycle progression in these intestinal cells. Flow cytometry analysis revealed that PTHrP treatment diminishes the number of cells in the G0/G1 phase and increases the number in both S and G2/M phases. The hormone increases the expression of CDK6 and diminishes the amount of negative cell cycle regulators p27Kip1, p15INK4B, and p53. However, PTHrP does not modify the expression of cyclin D3, CDK4, and p16INK4A. In addition, inhibitors of ERK1/2 (PD98059), p38 MAPK (SB203580), and PI3Kinase (LY294002) reversed PTHrP response in Caco-2 cells. Taken together, our results suggest that PTHrP positively modulates cell cycle progression and changes the expression of proteins involved in cell cycle regulation via ERK1/2, p38 MAPK, and PI3K signaling pathways in Caco-2 cells.
      PubDate: Wed, 25 Jun 2014 07:00:00 GMT
  • Lessons from a red squirrel, mentors, and the pathway to success
    • Authors: Reinhart A.F. Reithmeier
      Abstract: Biochemistry and Cell Biology, e-First Articles. In this article I will review my personal career path starting with how a red squirrel got me interested in research, and the vital role that mentors played in my pathway to success — a pathway that taught me many lessons that I would like to share with the reader, particularly graduate students and post-doctoral fellows who are just starting down their own unique pathways.
      PubDate: Mon, 23 Jun 2014 07:00:00 GMT
  • Differential nuclear shape dynamics of invasive andnon-invasive breast
           cancer cells are associated with actin cytoskeleton organization and
    • Authors: Rena Chiotaki; Hara Polioudaki, Panayiotis A. Theodoropoulos
      Abstract: Biochemistry and Cell Biology, e-First Articles. Cancer cells often exhibit characteristic aberrations in their nuclear architecture, which are indicative of their malignant potential. In this study, we have examined the nuclear and cytoskeletal composition, attachment configuration dynamics, and osmotic or drug treatment response of invasive (Hs578T and MDA-MB-231) and non-invasive (MCF-10A and MCF-7) breast cancer cell lines. Unlike MCF-10A and MCF-7, Hs578T and MDA-MB-231 cells showed extensive nuclear elasticity and deformability and displayed distinct kinetic profiles during substrate attachment. The nuclear shape of MCF-10A and MCF-7 cells remained almost unaffected upon detachment, hyperosmotic shock, or cytoskeleton depolymerization, while Hs578T and MDA-MB-231 revealed dramatic nuclear contour malformations following actin reorganization.
      PubDate: Tue, 17 Jun 2014 07:00:00 GMT
  • A novel role of transient receptor potential mucolipin1 (TRPML1) in
           protecting against imidazole-induced cytotoxicity
    • Authors: Zhenxing Liu; Shuan Zhao, Shuaishuai Wu, Jingyou Zhang, Zunyang Nie, Shenming Zeng
      Abstract: Biochemistry and Cell Biology, e-First Articles. Lysosomotropic amines cause serious side effects such as cytoplasmic vacuolation and cell death. TRPML1 (also known as mucolipin1), a member of the transient receptor potential (TRP) protein family, may regulate fusion/fission of vesicles along the endocytic pathway and some aspects of lysosomal ion homeostasis. Nevertheless, it is still unknown whether TRPML1 is involved in death of mammalian cells induced by lysosomotropic agents. In this study, imidazole was used as a model to investigate the role of TRPML1 in the cytotoxicity of lysosomotropic agents. Overexpression of wild-type TRPML1 inhibited imidazole-induced vacuole formation and cell death in human endometrial adenocarcinoma (HEC-1B) cells. In contrast, siRNA-mediated TRPML1 knockdown increased the cell death induced by imidazole. Bafilomycin A1 raises the pH of acidic organelles and therefore suppresses accumulation of weak bases in them. Similarly, lysosomal pH was raised in TRPML1-overexpressing cells; therefore, we inferred that TRPML1 protected against imidazole toxicity by regulating the pH of acidic organelles. We concluded that TRPML1 had a novel role in protecting against lysosomotropic amine toxicity.
      PubDate: Wed, 28 May 2014 07:00:00 GMT
  • Protein transport into the human ER and related diseases,
    • Authors: Sarah Haßdenteufel; Marie-Christine Klein, Armin Melnyk, Richard Zimmermann
      Abstract: Biochemistry and Cell Biology, e-First Articles. Protein transport into the human endoplasmic reticulum (ER) is relevant to the biogenesis of most soluble and membrane proteins of organelles, which are involved in endo- or exo-cytsosis. It involves amino-terminal signal peptides in the precursor polypeptides and various transport components in the cytosol plus the ER, and can occur co- or post-translationally. The two mechanisms merge at the level of the ER membrane, specifically at the level of the heterotrimeric Sec61 complex, which forms a dynamic polypeptide-conducting channel in the ER membrane. Since the mammalian ER is also the main intracellular calcium storage organelle, and the Sec61 complex is calcium permeable, the Sec61 complex is tightly regulated in its equilibrium between the closed and open conformations, or “gated”, by ligands, such as signal peptides of the transport substrates and the ER lumenal Hsp70-type molecular chaperone BiP. Furthermore, BiP binding to the incoming polypeptide contributes to the efficiency and unidirectionality of transport. Recent insights into the structure and dynamic equilibrium of the Sec61 complex have various mechanistic as well as medical implications.
      PubDate: Tue, 27 May 2014 07:00:00 GMT
  • Small expression tags enhance bacterial expression of the first three
           transmembrane segments of the apelin receptor
    • Authors: Aditya Pandey; Muzaddid Sarker, Xiang-Qin Liu, Jan K. Rainey
      Abstract: Biochemistry and Cell Biology, e-First Articles. G-protein coupled receptors (GPCRs) are inherently dynamic membrane protein modulators of various important cellular signaling cascades. The apelin receptor (AR or APJ) is a class A GPCR involved in numerous physiological processes, implicated in angiogenesis during tumour formation and as a CD4 co-receptor for entry of human immunodeficiency virus type 1 (HIV-1) to cells. Due to the lack of efficient methods to produce full-length GPCRs enriched with nuclear magnetic resonance (NMR) active 15N, 13C, and (or) 2H isotopes, small GPCR fragments typically comprising 1–2 transmembrane segments are frequently studied using NMR spectroscopy. Here, we report successful overexpression of transmembrane segments 1–3 of AR (AR_TM1-3) in the C41(DE3) strain of Escherichia coli using an AT-rich gene tag previously reported to enhance cell-free expression yields. The resulting protein, with 6 additional N-terminal residues due to the expression tag, was purified using high-performance liquid chromatography (HPLC). Far UV circular dichroism spectropolarimetry demonstrates that AR_TM1-3 has the predicted ∼40% α-helical character in membrane-mimetic environments. 1H-15N HSQC NMR experiments imply amenability to high-resolution NMR structural characterization and stability in solution for weeks. Notably, this small expression tag approach may also be generally applicable to other membrane proteins that are difficult to express in E. coli.
      PubDate: Fri, 23 May 2014 07:00:00 GMT
  • Dual cross-linking ribonucleoprotein immunoprecipitation assay
    • Authors: Dilshad H. Khan; James R. Davie
      Abstract: Biochemistry and Cell Biology, e-First Articles. Ribonucleoprotein immunoprecipitation (RIP) is an antibody-based method to detect RNA–protein interactions in situ. In the assay, UV cross-linking is commonly used to preserve RNA–protein interactions for subsequent target identification. UV light is a zero-length cross linker and thus identifies proteins directly bound to RNAs. Here, we describe a dual cross-linking RIP method that involves sequential protein–protein cross-linking step with a protein–protein cross-linker, followed by protein–RNA fixation by UV irradiation. In this way, proteins that indirectly bound to RNA can be analyzed.
      PubDate: Thu, 22 May 2014 07:00:00 GMT
  • Comparison of the adipogenesis in intramuscular and subcutaneous
           adipocytes from Bamei and Landrace pigs
    • Authors: Guo Hua Zhang; Jian Xiong Lu, Yan Chen, Yong Qing Zhao, Peng Hui Guo, Ju Tian Yang, Rong Xin Zang
      Abstract: Biochemistry and Cell Biology, e-First Articles. Fat deposition is a complex process involving proliferation, differentiation, and lipogenesis of adipocytes. Bamei and Landrace are considered to represent fat- and lean-type pig breeds. Subcutaneous (SC) and intramuscular (IM) pre-adipocytes were cultured to compare the proliferation and lipogenesis in these breeds. The differentiated adipocytes were exposed to glucose or insulin to evaluate their effects on lipogenesis and lipogenic gene expression. Pre-adipocytes proliferated dramatically faster in SC vs. IM cells, and in Bamei vs. Landrace breeds. Lipogenesis and lipogenic gene expression had a greater increase in Bamei than in Landrace, and in SC vs. IM in the process of differentiation. Glucose markedly promoted lipogenesis and lipogenic gene expression in differentiated adipocytes. The stimulation of high-glucose levels on lipogenesis and ChREBP and lipogenic gene expression was higher in SC than IM adipocytes, and in Bamei vs. Landrace. Insulin largely increased SREBP-1c expression, however it modestly stimulated lipogenesis and lipogenic gene expression, and there was no difference between cell populationsor between breeds. These data demonstrated that regional and varietal differences obviously existed in the development of porcine adipocytes. The proliferation and differentiation capacity of pre-adipocytes, and the adipocyte lipogenesis stimulated by glucose, are stronger in Bamei than Landrace, and in SC vs. IM adipocytes independent of breed.
      PubDate: Thu, 22 May 2014 07:00:00 GMT
  • Import of ribosomal proteins into yeast mitochondria
    • Authors: Michael W. Woellhaf; Katja G. Hansen, Christoph Garth, Johannes M. Herrmann
      Abstract: Biochemistry and Cell Biology, e-First Articles. Mitochondrial ribosomes of baker’s yeast contain at least 78 protein subunits. All but one of these proteins are nuclear-encoded, synthesized on cytosolic ribosomes, and imported into the matrix for biogenesis. The import of matrix proteins typically relies on N-terminal mitochondrial targeting sequences that form positively charged amphipathic helices. Interestingly, the N-terminal regions of many ribosomal proteins do not closely match the characteristics of matrix targeting sequences, suggesting that the import processes of these proteins might deviate to some extent from the general import route. So far, the biogenesis of only two ribosomal proteins, Mrpl32 and Mrp10, was studied experimentally and indeed showed surprising differences to the import of other preproteins. In this review article we summarize the current knowledge on the transport of proteins into the mitochondrial matrix, and thereby specifically focus on proteins of the mitochondrial ribosome.
      PubDate: Tue, 20 May 2014 07:00:00 GMT
  • Mechanism of a novel missense mutation, p.V174M, of the human connexin31
           (GJB3) in causing nonsyndromic hearing loss
    • Authors: Tung-Cheng Li; Yu-Hsiang Kuan, Tzu-Yu Ko, Chuan Li, Jiann-Jou Yang
      Abstract: Biochemistry and Cell Biology, e-First Articles. Hearing loss is the most common sensory disorder, worldwide. In a recent study, we have identified a missense mutation, p.V174M, in the connexin 31 encoded by the GJB3 gene, in a patient with nonsyndromic hearing loss. However, the functional change in the CX31V174M mutant remains unknown. This study compared the intracellular distribution and assembly of the mutant CX31V174M with that of the wild-type (WT) CX31 in HeLa cells, and it examined the effect that the mutant protein had on those cells. A fluorescent localization assay of WT CX31 showed the typical punctuate pattern of a gap junction channel between the neighboring expression cells. Conversely, the p.V174M missense mutation resulted in the accumulation of the mutant protein in the lysosomes rather than in the cytoplasmic membrane. Moreover, dye transfer experiments have also demonstrated that the CX31V174M mutant did not form functional gap junction channels, probably due to the incorrect assembly or the altered properties of the CX31 channels. In addition, we found that CX31V174M-transfection can cause cell death by MTT assay. CX31V174M co-expressed with either CX31WT or CX26WT studies, suggested the impairment of the ability of CX26WT proteins to intracellular trafficking and targeting to the plasma membrane, but did not influence the trafficking of CX31WT. Based on these findings, we suggest that the CX31V174M mutant may have an effect on the formation and function of the gap junction, and CX31V174M has a trans-dominant negative effect on the function of wild types CX26. These results provide a novel molecular explanation for the role that GJB3 plays in hearing loss.
      PubDate: Thu, 15 May 2014 07:00:00 GMT
  • Ganglioside GM3 is required for caffeic acid phenethyl ester-induced
           megakaryocytic differentiation of human chronic myelogenous leukemia K562
    • Authors: Un-Ho Jin; Tae-Wook Chung, Kwon-Ho Song, Choong-Hwan Kwak, Hee-Jung Choi, Ki-Tae Ha, Young-Chae Chang, Young-Choon Lee, Cheorl-Ho Kim
      Abstract: Biochemistry and Cell Biology, e-First Articles. The human chronic myelogenous cell line K562 has been used extensively as a model for the study of leukemia differentiation. We show here that treatment of K562 cells with caffeic acid phenethyl ester (CAPE) induced a majority of cells to differentiate towards the megakaryocytic lineage. Microscopy analysis showed that K562 cells treated with CAPE exhibited characteristic features of physiological megakaryocytic differentiation, including the presence of vacuoles and demarcation membranes. Differentiation of K562 cells treated with CAPE was also accompanied by a net increase in megakaryocytic markers. The transcriptional activity of lactosylceramide α-2,3-sialyltransferase (GM3 synthase) and synthesis of ganglioside GM3 were increased by CAPE treatment. The promoter analysis of GM3 synthase demonstrated that CAPE induced the expression of GM3 synthase mRNA via activation of the cAMP response element-binding protein (CREB), transcription factor in nucleus. Interestingly, the inhibition of ganglioside GM3 synthesis by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propranol (D-PDMP) and GM3 synthase-siRNA blocked the CAPE-induced expression of the megakaryocytic markers and differentiation of K562 cells. Taken together, these results suggest that CAPE induces ganglioside GM3-mediated megakaryocytic differentiation of human chronic myelogenous cells.
      PubDate: Tue, 13 May 2014 07:00:00 GMT
  • Functional expression of the Acanthamoeba castellanii alternative oxidase
           in Escherichia coli; regulation of the activity and evidence for Acaox
           gene function
    • Authors: Nina Antos-Krzeminska; Wieslawa Jarmuszkiewicz
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 235-241, June 2014. To evidence Acanthamoeba castellanii alternative oxidase (AcAOX) gene product function, we studied alterations in the levels of mRNA and protein and AcAOX activity during growth in amoeba batch culture. Moreover, heterologous expression of AcAOX in AOX-deficient Escherichia coli confirmed by the protein immunodetection and functional studies was performed. Despite the presence of native bo and bd quinol oxidases in E. coli membrane, from which the latter is known to be cyanide-resistant, functional expression of AcAOX in E. coli conferred cyanide-resistant benzohydroxamate-sensitive respiration on the bacteria. Moreover, AcAOX activity in transformed bacteria was stimulated by GMP and inhibited by ATP, indicating that AcAOX is regulated by mutual exclusion of purine nucleotides, which was previously demonstrated in the mitochondria of A. castellanii.
      PubDate: Mon, 05 May 2014 07:00:00 GMT
  • Myostatin inhibits proliferation and insulin-stimulated glucose uptake in
           mouse liver cells
    • Authors: Rani Watts; Mostafa Ghozlan, Curtis C. Hughey, Virginia L. Johnsen, Jane Shearer, Dustin S. Hittel
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 226-234, June 2014. Although myostatin functions primarily as a negative regulator of skeletal muscle growth and development, accumulating biological and epidemiological evidence indicates an important contributing role in liver disease. In this study, we demonstrate that myostatin suppresses the proliferation of mouse Hepa-1c1c7 murine-derived liver cells (50%; p < 0.001) in part by reducing the expression of the cyclins and cyclin-dependent kinases that elicit G1-S phase transition of the cell cycle (p < 0.001). Furthermore, real-time PCR-based quantification of the long noncoding RNA metastasis associated lung adenocarcinoma transcript 1 (Malat1), recently identified as a myostatin-responsive transcript in skeletal muscle, revealed a significant downregulation (25% and 50%, respectively; p < 0.05) in the livers of myostatin-treated mice and liver cells. The importance of Malat1 in liver cell proliferation was confirmed via arrested liver cell proliferation (p < 0.05) in response to partial Malat1 siRNA-mediated knockdown. Myostatin also significantly blunted insulin-stimulated glucose uptake and Akt phosphorylation in liver cells while increasing the phosphorylation of myristoylated alanine-rich C-kinase substrate (MARCKS), a protein that is essential for cancer cell proliferation and insulin-stimulated glucose transport. Together, these findings reveal a plausible mechanism by which circulating myostatin contributes to the diminished regenerative capacity of the liver and diseases characterized by liver insulin resistance.
      PubDate: Thu, 24 Apr 2014 07:00:00 GMT
  • Interaction of Grb2 SH3 domain with UVRAG in an Alzheimer’s
           disease–like scenario
    • Authors: Kasturi Roy; Oishee Chakrabarti, Debashis Mukhopadhyay
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 219-225, June 2014. Growth factor receptor-bound protein 2 (Grb2) is an adaptor protein which participates in trafficking pathways alongside its role in signaling. Proteins important for actin remodeling and cellular compartmentalization contain SRC Homology 3 (SH3) binding motifs that interact with Grb2. While studying the Grb2–amyloid precursor protein (APP) intracellular domain (AICD) interaction in Alzheimer’s disease cell line models, it was seen that Grb2 colocalized to compartments that mature into autophagosomes. The entrapping of AICD in the Grb2 vesicles and its clearance via autophagosomes was a survival contrivance on the part of the cell. Here, we report that Grb2, when in excess, interacts with ultraviolet radiation resistance-associated gene protein (UVRAG) under excess conditions of AICD–Grb2 or Grb2. The N-terminal SH3 domain of Grb2 specifically interacts with UVRAG, unlike the C-terminal SH3 domain. This interaction helps to understand the role of Grb2 in the autophagic maturation of vesicles.
      PubDate: Thu, 24 Apr 2014 07:00:00 GMT
  • Targeting angiogenic pathway for chemoprevention of experimental colon
           cancer using C-phycocyanin as cyclooxygenase-2 inhibitor
    • Authors: Manpreet Kaur Saini; Sankar Nath Sanyal
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 206-218, June 2014. An angiogenic pathway was studied that involved stromal tissue degradation with matrix metalloproteinases (MMPs), vesicular endothelial growth factor-A (VEGF-A), and hypoxia inducible factor-1α (HIF-1α) mediated growth regulation in a complex interaction with chemokines, such as monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1β (MIP-1β). Gene and protein expression was studied with real-time PCR, Western immunoblot, and immunofluorescence. Morphological and histopathological analysis of tumor was done, as also the activity of MMPs and HIF-1α by gelatin zymography and ELISA. Binding interactions of proteins were studied by molecular docking. Piroxicam, a traditional NSAID and C-phycocyanin, a biliprotein from Spirulina platensis, were utilized in the chemoprevention of DMH-induced rat colon cancer. A significant number of tumors was evident in DMH treated animals, while with piroxicam and C-phycocyanin, the number and size of tumors/lesions were reduced. Colonic tissues showed severe dysplasia, tubular adenoma, and adenocarcinoma from DMH, with invasive features along with signet ring cell carcinoma. No occurrence of carcinoma was detected in either of the drug treatments or in a combination regimen. An elevated VEGF-A, MMP-2, and MMP-9 level was observed, which is required for metastasis and invasion into surrounding tissues. Drugs induced chemoprevention by down-regulating these proteins. Piroxicam docked in VEGF-A binding site of VEGF-A receptors i.e., VEGFR1 and VEGFR2, while phycocyanobilin (a chromophore of C-phycocyanin) docked with VEGFR1 alone. HIF-1α is up-regulated which is associated with increased oxygen demand and angiogenesis. MCP-1 and MIP-1β expression was also found altered in DMH and regulated by the drugs. Anti-angiogenic role of piroxicam and C-phycocyanin is well demonstrated.
      PubDate: Thu, 24 Apr 2014 07:00:00 GMT
  • Cationic lipid nanodisks as an siRNA delivery vehicle
    • Authors: Mistuni Ghosh; Gang Ren, Jens B. Simonsen, Robert O. Ryan
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 200-205, June 2014. The term nanodisk (ND) describes reconstituted high-density lipoprotein particles that contain one or more exogenous bioactive agents. In the present study, ND were assembled from apolipoprotein A-I, the zwitterionic glycerophospholipid 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC), and the synthetic cationic lipid 1,2-dimyristoyl-3-trimethylammonium-propane (DMTAP). ND formulated at a DMPC:DMTAP ratio of 70:30 (by weight) were soluble in aqueous media. The particles generated were polydisperse, with diameters ranging from ∼20 to
      PubDate: Tue, 22 Apr 2014 07:00:00 GMT
  • Role of Nodal–PITX2C signaling pathway in glucose-induced
           cardiomyocyte hypertrophy
    • Authors: Dongmei Su; Sun Jing, Lina Guan, Qian Li, Huiling Zhang, Xiaobo Gao, Xu Ma
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 183-190, June 2014. Pathological cardiac hypertrophy is a major cause of morbidity and mortality in cardiovascular disease. Recent studies have shown that cardiomyocytes, in response to high glucose (HG) stimuli, undergo hypertrophic growth. While much work still needs to be done to elucidate this important mechanism of hypertrophy, previous works have showed that some pathways or genes play important roles in hypertrophy. In this study, we showed that sublethal concentrations of glucose (25 mmol/L) could induce cardiomyocyte hypertrophy with an increase in the cellular surface area and the upregulation of the atrial natriuretic peptide (ANP) gene, a hypertrophic marker. High glucose (HG) treatments resulted in the upregulation of the Nodal gene, which is under-expressed in cardiomyocytes. We also determined that the knockdown of the Nodal gene resisted HG-induced cardiomyocyte hypertrophy. The overexpression of Nodal was able to induce hypertrophy in cardiomyocytes, which was associated with the upregulation of the PITX2C gene. We also showed that increases in the PITX2C expression, in response to Nodal, were mediated by the Smad4 signaling pathway. This study is highly relevant to the understanding of the effects of the Nodal–PITX2C pathway on HG-induced cardiomyocyte hypertrophy, as well as the related molecular mechanisms.
      PubDate: Fri, 28 Mar 2014 07:00:00 GMT
  • Dynamics of WD-repeat containing proteins in SSU processome components
    • Authors: Kouko Wada; Manae Sato, Nanase Araki, Masahiro Kumeta, Yuya Hirai, Kunio Takeyasu, Kazuhiro Furukawa, Tsuneyoshi Horigome
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 191-199, June 2014. Nine WD-repeat containing proteins in human SSU processome components have been found in a HeLa cell nuclear matrix fraction. In these proteins, t-UTP sub-complex components, i.e., CIRH1A, UTP15, and WDR43, were shown to be immobilized in the fibrillar centers of nucleoli in living cells. In this study, the dynamics of the remaining six proteins fused with green fluorescent protein (GFP), i.e., PWP2-GFP, TBL3-GFP, GFP-UTP18, GFP-NOL10, GFP-WDR46, and GFP-WDSOF1, were examined in living cells. The findings were as follows. (i) The majority of UTP-B sub-complex components, i.e., PWP2-GFP, TBL3-GFP, and GFP-UTP18, are localized to the dense fibrillar component and granular component regions in nucleoli; (ii) When rRNA transcription is suppressed, the majority of GFP-fused UTP-B sub-complex components are localized in the cap and body regions of nucleoli. (iii) The mobility of these proteins except for GFP-WDSOF1, and half of GFP-UTP18 and GFP-WDR46, respectively, is very low in living cells. (iv) When rRNA transcription is suppressed, the mobility of these proteins except for GFP-WDSOF1 is accelerated but still slow. These findings and others suggest that these WD-repeat proteins other than GFP-WDSOF1 found in the nuclear matrix fraction bind tightly to some macro-protein complexes and act as a scaffold or a core for the complexes in nucleoli.
      PubDate: Thu, 27 Mar 2014 07:00:00 GMT
  • BMP and activin membrane-bound inhibitor (BAMBI) inhibits the adipogenesis
           of porcine preadipocytes through Wnt/β-catenin signaling pathway
    • Authors: Yin Mai; Zhenyu Zhang, Hao Yang, Peiyue Dong, Guiyan Chu, Gongshe Yang, Shiduo Sun
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 172-182, June 2014. The process of differentiation from preadipocytes to adipocytes contributes to adipose tissue expansion in obesity. Blocking adipogenesis may be conducive to the etiology of obesity-related diseases. BMP and activin membrane-bound inhibitor (BAMBI) is a transmembrane protein, which was identified as a target of β-catenin in colorectal and hepatocellular tumor cells. However, whether BAMBI affects adipogenesis by Wnt/β-catenin signaling remains to be explored. In this study, we distinguish BAMBI as an inhibitor of preadipocytes differentiation. We found that BAMBI was downregulated during preadipocytes differentiation. Knockdown of BAMBI increased adipogenesis and blocked Wnt/β-catenin signaling by repressing β-catenin accumulation. In BAMBI overexpression cells, lipid accumulation was reduced by promoting nuclear translocation of β-catenin. Lithium chloride (LiCl) is an activator of Wnt/β-catenin signaling, which is an inhibitor of glycogen synthetase kinase-3 (GSK-3), maintaining the stability of β-catenin in cytosolic. We showed BAMBI strengthened the anti-adipogenic effects of LiCl. In addition, the results indicated that BAMBI was upregulated by β-catenin. These observations illuminated that BAMBI inhibits adipogenesis by a feedback loop (BAMBI→β-catenin nuclear translocation→BAMBI), which forms with Wnt/β-catenin signaling.
      PubDate: Wed, 26 Mar 2014 07:00:00 GMT
  • A new mechanism in the binding between Homer3 EVH1 domain and inositol
           1,4,5 trisphosphate receptor suppressor domain
    • Authors: He Wen; Hyuk Nam Kwon, Sunghyouk Park
      Abstract: Biochemistry and Cell Biology, Volume 92, Issue 3, Page 163-171, June 2014. The suppressor domain of inositol 1,4,5 trisphosphate receptor (IP3R) has critical roles in regulating the calcium channel by interacting with many binding partners. The residue 49–53 (PPKKF) of the suppressor domain was suggested to be a canonical Homer EVH1 domain binding site and is also the first a part of calmodulin (CaM) binding site. As CaM-binding of the suppressor domain has been shown to involve large-scale conformational changes, we studied the binding characteristics of the Homer EVH1-suppressor domain with NMR spectroscopy and biochemical pull-down assays for mutants. Our data show that the suppressor domain employs the PPKKF motif in a similar but subtly different way compared to previously characterized interactions, and that the suppressor domain does not undergo large-scale conformational changes. Chemical shift assignments of the Homer3 EVH1 domain found that a new set of residues, located at the opposite side of the previously reported binding site, is also involved in binding, which was confirmed by mutant binding assays. Further analysis suggests that F40 in the new binding sites may have a critical role as a conformational lock-switch in Homer-target binding. The proposed mechanism is implicated in the signaling network involving calcium channels.
      PubDate: Mon, 10 Mar 2014 07:00:00 GMT
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