Relevant bibliographies by topics / 060802 Animal Cell and Molecular Biology

Academic literature on the topic '060802 Animal Cell and Molecular Biology'

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Journal articles on the topic "060802 Animal Cell and Molecular Biology"

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Wright, G. J. "Animal magic uncloaked: Molecular Principles of Animal Development." Journal of Cell Science 116, no. 1 (January 1, 2003): 5—a—6. http://dx.doi.org/10.1242/jcs.00188.

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Ghose, Piya, and Shai Shaham. "Cell death in animal development." Development 147, no. 14 (July 15, 2020): dev191882. http://dx.doi.org/10.1242/dev.191882.

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ABSTRACTCell death is an important facet of animal development. In some developing tissues, death is the ultimate fate of over 80% of generated cells. Although recent studies have delineated a bewildering number of cell death mechanisms, most have only been observed in pathological contexts, and only a small number drive normal development. This Primer outlines the important roles, different types and molecular players regulating developmental cell death, and discusses recent findings with which the field currently grapples. We also clarify terminology, to distinguish between developmental cell death mechanisms, for which there is evidence for evolutionary selection, and cell death that follows genetic, chemical or physical injury. Finally, we suggest how advances in understanding developmental cell death may provide insights into the molecular basis of developmental abnormalities and pathological cell death in disease.
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Takeichi, M. "The cadherins: cell-cell adhesion molecules controlling animal morphogenesis." Development 102, no. 4 (April 1, 1988): 639–55. http://dx.doi.org/10.1242/dev.102.4.639.

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Cadherins are a family of glycoproteins involved in the Ca2+-dependent cell-cell adhesion mechanism which is detected in most kinds of tissues. Inhibition of the cadherin activity with antibodies induces dissociation of cell layers, indicating a fundamental importance of these molecules in maintaining the multicellular structure. Cadherins are divided into subclasses, including E-, N- and P-cadherins. While all subclasses are similar in molecular weight, Ca2+- and protease-sensitivity, each subclass is characterized by a unique tissue distribution pattern and immunological specificity. Analysis of amino acid sequences deduced from cDNA encoding these molecules showed that they are integral membrane proteins of 723–748 amino acids long and share common sequences; similarity in the sequences between subclasses is in a range of 50–60% when compared within a single animal species. L cells, with very little endogenous cadherin activity, transfected with the cadherin cDNA acquired high cadherin-mediated aggregating activity. Their colony morphology was altered by the ectopic expression of cadherins from the dispersed type to the compact type, providing direct evidence for a key role of cadherins in cell-cell adhesion. It has been suggested that cadherins bind cells by their homophilic interactions at the extracellular domain and are associated with actin bundles at the cytoplasmic domain. It appears that each cadherin subclass has binding specificity and this molecular family is involved in selective cell-cell adhesion. In development, the expression of each cadherin subclass is spatiotemporally regulated and associated with a variety of morphogenetic events; e.g. the termination or initiation of expression of a cadherin subclass in a given cell collective is correlated with its segregation from or connection with other cell collectives. Antibodies to cadherins were shown to perturb the morphogenesis of some embryonic organs in vitro. These observations suggest that cadherins play a crucial role in construction of tissues and the whole animal body.
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KNIGHT, D., G. SHAH, and G. GOUGH. "Methods in molecular biology, vol. 5: Animal cell cultures." Trends in Biotechnology 8 (1990): 371. http://dx.doi.org/10.1016/0167-7799(90)90237-r.

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Clynes, M. "Animal cell culture (methods in molecular biology, volume 5)." FEBS Letters 287, no. 1-2 (August 5, 1991): 231. http://dx.doi.org/10.1016/0014-5793(91)80066-c.

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Burridge, A. "Molecular Principles of Animal Development." International Journal of Biochemistry & Cell Biology 35, no. 1 (January 2003): 111. http://dx.doi.org/10.1016/s1357-2725(02)00073-0.

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Moss, Eric G., and Jennifer Romer-Seibert. "Cell-intrinsic timing in animal development." Wiley Interdisciplinary Reviews: Developmental Biology 3, no. 5 (July 24, 2014): 365–77. http://dx.doi.org/10.1002/wdev.145.

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Merten, Otto-Wilhelm. "Animal cell culture: A practical approach." Trends in Biochemical Sciences 11, no. 10 (October 1986): 412. http://dx.doi.org/10.1016/0968-0004(86)90170-2.

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Bliem, Rudolf F. "Animal cell technology — principles and products." Trends in Biochemical Sciences 13, no. 8 (August 1988): 325–26. http://dx.doi.org/10.1016/0968-0004(88)90134-x.

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Ricci, Lorenzo, and Mansi Srivastava. "Wound-induced cell proliferation during animal regeneration." Wiley Interdisciplinary Reviews: Developmental Biology 7, no. 5 (May 2, 2018): e321. http://dx.doi.org/10.1002/wdev.321.

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Dissertations / Theses on the topic "060802 Animal Cell and Molecular Biology"

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Siam, Rania. "Mechanisms of C. crescentus regulation of chromosome replication by a cell cycle regulator protein." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37838.

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Caulobacter crescentus divides asymmetrically to produce two different progeny, a swarmer progeny that is replication incompetent, and a stalked cell progeny that is replication competent. Upon cell division, a cell cycle regulator protein (CtrA) was identified only in the swarmer cells, and additional circumstantial evidence links this protein to being a repressor of chromosome replication. For example, this response regulator protein binds to five specific sites in the replication origin (Cori) designated [a-e]. We carefully studied the binding characteristics of both phosphorylated (CtrA~P) and unphosphorylated forms of the protein to the five binding sites [a-e] in the replication origin (Chapter 2) and upstream of the ctrA gene (Chapter 3). We showed that phosphorylation significantly enhances binding affinity in the replication origin (Chapter 2) but not upstream of ctrA (Chapter 3). In addition a "pseudo-active" protein form (CtrA D51E) that resembles the phosphorylated form in vivo did not improve the binding characteristics (Chapter 3). These results suggest that enhanced binding on phosphorylation is not the only signal achieved on phosphorylation. In fact, CtrA half-site mutation binding studies shows that phosphorylation stimulates protein/protein interaction and cooperative binding between sites [a] and [b] in the replication origin (Chapter 2). We show that CtrA binding site [b] is the major contributor in the cooperative CtrA binding between [a] and [b] (Chapter 4). We demonstrate that cooperative binding of CtrA~P to sites [a] and [b] repress transcription from a strong promoter (Ps), which in turn blocks plasmid replication. In addition, mutating site [b] to block CtrA binding to [a] and [b] has a deleterious effect on chromosome replication (Chapter 4).
This cooperative CtrA binding at [a] and [b] is independent from the upstream binding sites [c-e] (Chapter 2). CtrA∼P binding in the origin is altered in the presence of the histone-like protein (IHF) that also binds and overlaps CtrA binding site [c] (Chapter 5). In-fact, IHF binds and overlaps binding site [c] (Chapter 5). We propose a replication model in the stalked cell were IHF binding hinders active CtrA binding in the replication origin and regulates cooperative transcription that coincides with replication initiation.
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Nguyen, Hannah Anh-Quan. "Regulation of gene expression and cell growth by transcriptional proteins of the interferon system." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35028.

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The Interferon Regulatory Factors (IRFs) are a family of interferon-inducible proteins which play distinct roles in diverse processes such as pathogen response, cytokine signalling, cell growth regulation and hematopoietic development. The objective of this research was to investigate the mechanisms by which IRF-1 and IRF-2 regulate gene expression and cell growth. Structure-function analyses of the IRF-2 protein demonstrate that transcriptional repression by IRF-2 is contained within the first 125 N-terminal amino acids and correlates directly with IRF-2 DNA binding. Overexpression of functional IRF-2 deletion mutant proteins in NIH3T3 cells results in oncogenic transformation and tumorigenesis, suggesting that IRF-2 oncogenicity correlates directly with transcriptional repression. Similar structure-function analyses localize IRF-1 transactivation to the C-terminus. Like IRF-1, hybrid constructs which fuse the DNA binding domain of IRF-1 and IRF-2 to the transactivation domain of NF-kappaB RelA(p65) are transcriptional activators. Inducible expression of IRF-1 and IRF/RelA in NIH3T3 cells results in reduced cellular growth and induction of apoptosis. Furthermore, expression of the PKR, STAT1(p91), and WAF1 growth regulatory proteins are elevated following induction of IRF-1 or IRF/RelA, correlating transactivation function and tumor suppressor activity of IRF-1 or IRF/RelA. By RNA fingerprinting, the secretory leukocyte protease inhibitor (SLPI) was identified as the first gene whose expression is downregulated by IRF-1 or IRF-1/RelA. A region in the SLPI promoter was identified that bound IRF-1, suggesting a direct mechanism for IRF-1 regulation of SLPI expression.
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Saleh, Maya. "Protein-protein interactions and cell signaling in the regulation of HOX.PBX functions." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37620.

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HOX proteins are homeodomain-containing transcription factors essential for embryonic patterning. Despite amino acid differences, all HOX homeodomains recognize highly similar sites on DNA. One mechanism by which HOX proteins achieve specificity is through interaction with cofactors of the PBX and MEIS/PREP1 families. Higher order complexes between HOX, PBX and MEIS/PREP1 proteins form in vivo and are essential for target recognition and transcriptional regulation. Another level of control of HOX function is the nuclear availability of its cofactors. This thesis addresses the regulation of the nuclear availability of the PBX protein by MEIS/PREP1 family members. We identified two nuclear localization signals (NLS) in the PBX homeodomain and showed that the NLS are masked in the absence of MEIS/PREP1. Upon a conformational change in PBX induced by MEIS/PREP1 binding, the NLS are exposed and a receptor-mediated active transport of PBX into the nucleus is allowed. This thesis also investigates the mechanisms of transcriptional regulation by the HOX·PBX complexes. We show that HOX·PBX complexes repress transcription and are switched to transcriptional activators in response to cell signaling. We demonstrate that PBX mediates the repression function by recruiting histone deacetylases (HDACs) to HOX target promoters. Inhibition of HDAC activity or stimulation of protein kinase A (PKA) signaling converts the HOX·PBX complex into a net activator of transcription. The activation function is mediated by the HOX protein through its recruitment of CREB-binding protein (CBP), a coactivator with histone acetyl-transferase (HAT) activity. We propose a model whereby HOX·PBX transcriptional activity is determined by cell signaling, and is mediated by the local modification of chromatin structure in the promoter of downstream targets.
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Brule, Veronique. "The role of RBF1 in animal survival and in male germline stem cell differentiation during Drosophila melanogaster development." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119514.

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Retinoblastoma (RB) is a tumour-suppressing protein involved in many cellular functions including: cell cycle regulation, cellular differentiation and cell death. In the past, its function has been intrinsically linked to its role in the cell cycle, wherein it acts as a key regulator of the G1 to S-phase transition checkpoint. However, evidence has emerged in support of cell cycle-independent roles for RB. In particular, it has been demonstrated that RB plays an important role in promoting normal animal development and survival to adulthood, a function that is conserved between mammals and metazoans. This role has been extensively studied using RBF1, the Drosophila melanogaster homolog of mammalian RB. An outstanding question in this field is whether or not the mutation of RB results in tissue-specific biological outcomes that ultimately affect adult viability. The results of this research thesis suggest that the mutation RBF1 can lead to tissue-specific developmental defects; however, the defects observed did not affect the ability of animals in surviving to adulthood. For example, a male germline-specific phenotype was observed when RBF1 expression was absent from germ cells. Adult male flies in which RBF1 expression was absent from the germline were sterile. Upon closer inspection, changes in germ cell number and patterning in the testes were observed. As well, an increase in cyclin E expression in RBF1-null mutants suggested that germ cells were being arrested at an early stage of spermatogenesis. A role for RBF1 in the fly germline has not been previously investigated. Therefore, this research project has identified a novel function of RBF1 with respect to germline regulation. Additionally, this research thesis also aimed to investigate whether RB interacted with a subset of known RB-associating factors in a tissue-specific manner. While this question was not completely addressed by the research presented herein, phosphorylation of Serine 728 on RBF1 was detected in vivo. This site was previously investigated in vitro and was suggested to be a putative phosphorylation target by cyclin/Cdk complexes. Therefore, the data of this research thesis have demonstrated the potential for this site to be phosphorylated in vivo. Further experimentation is required in order to verify the authenticity of this site as an endogenous target of phosphorylation. Overall, the data presented in this research thesis provide new insight into the various roles of RBF1 and the manner in which it is regulated.
Le rétinoblastome (RB) est une protéine classifiée comme suppresseur de tumeur. Elle joue plusieurs rôles importants dans la cellule, incluant: la régulation du cycle cellulaire, la différentiation cellulaire et l'apoptose. Dès sa découverte, le rétinoblastome a été caractérisé par son rôle primaire en règlant le cycle cellulaire dans lequel RB fonctionne comme régulateur de la transition entre la phase G1 et la phase S. Depuis ce temps, d'autres rôles pour RB indépendents de son fonctionnement dans le cycle cellulaire ont été identifiés. Notamment, il a été démontré que RB joue un rôle important dans la promotion de processus de dévelopement normal dans l'animal et la survie jusqu'à l'âge d'adulte. La plupart des recherches concentrant sur ce rôle ont été faites en utilisant la Drosophile, une espèce modèle qui convient à la manipulation génétique et en laquelle l'homologue de RB se nomme RBF1.Il reste plusieurs questions à rechercher à propos du rôle de RBF1 concernant la survie de l'animal jusqu'à l'âge d'adulte. Cette thèse essaie de répondre à la question suivante; est-ce que les effets biologiques résultant de mutater RBF1 sont spécifiques à des tissus particuliers, et est-ce qu'ils ont un effet sur l'abilité de la Drosophila de survivre jusqu'au stage d'adulte? Les résultats de cette thèse indiquent qu'en mutant RBF1, il est possible de produire des effets biologiques unique dans des tissus spécifiques. Quand même, aucun de ces effets ont affecté la survie de l'animal. Par example, il a été démontré que RBF1 joue un rôle unique dans le tissu gonade des mâles. Dans des Drosophiles qui n'expriment pas RBF1 dans les cellules de la lignée germinale, les adultes mâles étaient stériles. En examinant les testicules, le phénotype des cellules de la lignée germinale était différent en comparaison au phenotype sauvage. Aussi, le nombre de cellules da la lignée germinale qui expriment la cycline E avait augmenté. Précédemment, il n'y avait pas d'études qui ont recherché un rôle pour RBF1 dans la lignée germinale des Drosphiles mâles; donc, les résultats de cette thèse ont démontré un rôle unique pour RBF1 en régularisant la spermatogenèse dans les Drosophiles.En plus, cette thèse essaie de répondre à une autre question liée à celle ci-haut: est-ce que RB s'associe avec des macromolécules particulières (dont il est déjà connue à faire des associations), mais d'une manière unique à chaque tissu de la Drosophile? Les données de cette thèse ne donnent pas une réponse complète à cette question, mais elles ont identifié in vivo un site de phosphorylation (Sérine 728) sur RBF1. Ce site a déjà été recherché et a été suggéré in vitro d'être une cible de phosphorylation par les complexes Cdk-cyclines. Alors, les données présentées ci-haut démontrent que Sérine 728 peut être phosphorylé in vivo aussi. Plus de recherche est requis pour vérifier si ce site est un cible authentique de phosphorylation endogène in vivo. En conclusion, les données de cette thèse démontrent de nouvelles façons de régler le fonctionnement de RBF1, et elles présentent des informations nouvelles à propos des rôles variés de RBF1 dans la Drosophile.
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Knudson, Jennifer Caroline. "Cardiotrophin-1 as an ex vivo activator of a stem-cell like population in the murine heart." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26946.

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The identification of a multi-potent stem cell-like population (SP) within the adult murine heart infers new methods of cardiac repair, i.e. stem cells compensate for damage by generating new cardiomyocytes. Several studies have emphasized the dominance of the tissue microenvironment on the differentiation & functional properties of stem cells. Of particular interest was Cardiotrophin-1 (CT-1), a member of the Interleukin-6 (IL-6) family of cytokines. To assess whether CT-1 functioned as an activator of cardiac SP cells in the murine heart, an adenovirus containing the full length CT-1 driven by a ubiquitous promoter was generated. The adenovirus was administered via intra-cardiac injections and the effects of CT-1 were primarily assessed using fluorescence-activated cell sorting (FACS) analysis. Analysis showed a temporary increase in the cardiac SP of CT-1 injected hearts. A closer look at the SP cells in other tissues (liver, skeletal muscle and bone marrow) demonstrated that this phenomenon was cardiac specific. Interestingly the cardiac SP expressed the Leukemia Inhibitory Factor (LIF) receptor, which is required for CT-1 signaling through the 130 pathway. Protein analysis also showed that STAT3, a downstream member of the 130 pathway becomes activated in the heart during CT-1 injections. Preliminary results from co-culture experiments suggested that this increase was also accompanied by SP cell differentiation. These results proposed that CT-1 not only increased the cardiac SP size but may have also activated a cardiac differentiation program. The existence of a potential biologic stimulant (CT-1) for cardiac stem cells is an exciting prospect and offers support to the notion that cardiac repair may become a viable therapeutic option in the not too distant future.
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Wang, Yifang. "Role and regulation of X-linked inhibitor of apoptosis protein expression during development of the rat ovarian follicle in vitro." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/29006.

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Follicle stimulating hormone (FSH) is an important survival factor in the ovarian follicular development. Inhibitor of apoptosis proteins (IAPs) is a family of intracellular anti-apoptosic proteins. X-linked IAP (XIAP) has been shown to be involved in multiple biological activities (e.g. inhibition of caspase activities, promotion of ubiquitin-proteasome-mediated protein degradation, regulation of cell signaling pathways). The present thesis research project examines: (1) the role and gonadotropic regulation of XIAP expression in rat granulosa cells during ovarian follicular development and atresia; (2) the possible involvement of intra-ovarian factors such as transforming growth factor alpha (TGFalpha) in the FSH-induced XIAP expression and follicular development; and (3) the signal pathways involved in the gonadotropic up-regulation of XIAP during follicular development in vitro. A follicle culture system coupled to an adenoviral gene manipulation procedure has been established. FSH significantly increased follicular growth as evident by increases in follicular size, cell number and DNA contents in vitro. While cultured pre-antral or early-antral follicles showed a low XIAP content and evidence of apoptosis in the absence of FSH, gonadotropin addition increased XIAP content and suppressed apoptosis. At low FSH concentration, adenoviral XIAP sense cDNA expression increased follicular cell XIAP and DNA contents, reduced apoptosis, and enhanced follicular growth, while XIAP antisense elicited opposite responses. FSH-induced XIAP up-regulation appeared mediated, in part, by the secretion and action of follicular TGFalpha. In cultured rat follicles, FSH-stimulated estradiol production, TGFalpha secretion, XIAP expression and follicular growth were suppressed by intra-follicular injection of a neutralizing anti-TGFalpha antibody or addition of the estradiol antagonist ICI 182780 to the culture media. These results support my hypothesis that the FSH induces follicular growth by stimulating granulosa cell proliferation via theca TGFalpha secretion and action in response to increased granulosa cell estradiol synthesis. Since the promoter region of XIAP gene has nuclear kappa B (NFkappaB) binding site, it is possible that the transcription of XIAP is mediated via NFkappaB activation. FSH increased rat granulosa cell XIAP mRNA abundance and protein content. While the gonadotropin induced granulosa cell NFkappaB translocation from cytoplasm to nucleus and increased NFkappaB-DNA binding activity, pretreatment with an NFkappaB translocation inhibitor suppressed FSH-stimulated XIAP expression. (Abstract shortened by UMI.)
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Zhao, Qing 1966. "Prosaposin : a glycoprotein with multiple functions and dual destinations." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36857.

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Prosaposin is a multifunctional glycoprotein with different molecular masses and dual destinations. A 65 kDa form of prosaposin is targeted to lysosomes and converted by partial proteolysis, into four smaller non-enzymatic saposin A-D required for the hydrolysis of glycosphingolipids. However, the 65 kDa protein may be further glycosylated to a 70 kDa secretory form that is found in various biological fluids and suspected to have a trophic activity. Mutations of the prosaposin gene are linked to several lysosomal disorders. This thesis examines various aspects of the synthesis, targeting and function of prosaposin, and for practical purposes, the results and discussion were divided in three main sections. The first part deals with the cloning of the mouse prosaposin gene, the analysis of its transcribed mRNA and translation products. The second section examines the mechanism of targeting of the 65 kDa protein to lysosomes using mutagenic analyses. The third part deals with the effect of the inactivation of the prosaposin gene on the development of the male reproductive system. Sequence analysis revealed that the mouse prosaposin gene is over 20 kb in length and composed of 15 exons and 14 introns. Two forms of alternatively spliced mRNA (including or excluding exon 8) were found by RT-PCR in a tissue specific manner. Structure analysis and secondary structure predictions among mouse, rat and human prosaposins illustrated a common framework of amino acids forming amphiphatic helices enclosing an internal hydrophobic core implicated on their interaction with lipids. Mutagenic deletions of functional domains of prosaposin demonstrated that its C-terminus was required for the lysosomal targeting of this protein. Further evidence from chimeric constructs of albumin attached to various functional domains of prosaposin, suggested that the C-terminus plus at least one saposin domain are necessary for the targeting of albumin to lysosomes. Investigation of the effect of p
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An, Jing 1962. "Microenvironmental influences on the growth of normal and leukemic myeloid cells in the rat bone marrow." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41964.

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The hemopoietic microenvironment of the bone marrow is an essential regulator of in vivo hemopoiesis. In addition to supporting the growth of normal blood cells, it also influences the growth of leukemia. This thesis describes the use of a rat model to examine three aspects of the function of the hemopoietic microenvironment. First, using a myeloid leukemia cell line (BNML), we showed that the pattern of growth of these cells differed in the bone marrow and spleen, that their presence was associated with a relocalization of normal hemopoietic stem cells from marrow to spleen, and that factors (yet to be defined) released from spleen cells altered the pattern, possibly to create a more permissive environment. Second, we showed that the "ST3" marker of marrow fibroblasts was associated with the Thy-1 molecule, and either directly or indirectly contributed to the in vitro adhesion reaction between marrow fibroblastoid cells and normal and leukemic myeloid precursors. Third, we showed that ectopic bony ossicles induced by subcutaneous implantation of recombinant human bone morphogenetic protein-2 contained marrow expressing the full range of hemopoiesis, including stem cells with a potential for long-term repopulation (demonstrated using a rat Y-chromosome specific DNA probe that we developed), and contained fibroblastoid cells differentiated to express the ST3 antigen in a manner similar to those from femoral bone marrow. These results provide further evidence for, although not final proof of, the hypothesis that the ST3 antigen participates in the function of the rat hemopoietic microenvironment, and points the way to future experiments on the interactions between stromal elements and normal and leukemic myeloid precursors.
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Million, Passe Christina M. "Role and regulation of the high mobility group protein p8 in gonadotrope development, function, and tumorigenesis." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3330816.

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Thesis (Ph.D.)--Indiana University, Dept. of Biology, 2008.
Title from PDF t.p. (viewed on Jul 23, 2009). Source: Dissertation Abstracts International, Volume: 69-10, Section: B, page: 5924. Adviser: Christine Quirk.
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Springer, Lisa Nicole 1966. "Cellular and molecular mechanisms of 4-vinylcyclohexene-diepoxide induced ovotoxicity in rats." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282161.

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4-vinylcyclohexene diepoxide (VCD) is an environmental xenobiotic formed as a by-product in the manufacture of rubber and therefore potential human exposure is likely. VCD destroys half of the small pre-antral (25-100 μm) follicles in ovaries of rats following 15 days of dosing. The overall goal of this research, was to determine the mode and earliest time for identification of follicular destruction and examine the specificity of the response for 25-100 μm follicles. The particular involvement of protein synthesis and gene expression in this ovotoxic response was also examined. After daily dosing with VCD (80 mg/kg), the rate of protein synthesis in 25-100 μm follicles was inhibited following 3, 6, and 10 hr of in vitro incubation with VCD; whereas, the inhibition in the rate of protein synthesis at 3 hr in 25-100 μm follicles from untreated animals was reversed at 6 and 10 hr. Furthermore, follicular viability was compromised to a greater extent in 25-100 μm follicles from dosed versus untreated animals. Following 10 days of daily dosing with VCD, there was an increase in random DNA fragmentation in 25-100 μm follicles; however, there was not a reduction in the numbers of primordial and primary (25-100 μm) follicles. Morphological analysis showed changes characteristic of an apoptotic-like form of cell death in oocytes and granulosa cells of primordial and primary follicles 4 hr following 10 days of daily dosing. There was an increase in levels of mRNA for bax, manganese superoxide dismutase (MnSOD) and microsomal epoxide hydrolase (mEH) in 25-100 μm follicles following 10 days dosing with VCD, but the increase was not observed in large pre-antral (100-250 μm) follicles or liver. However, decreases in levels of mRNA for bax in liver and mEH in 100-250 μm follicles were observed. These results suggest that repeated dosing makes 25-100 μm follicles more susceptible to VCD-induced cellular changes and that VCD-induces an apoptotic-like form of cell death which is mediated through changes in levels of expression of genes associated with death of the follicular cells.
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Books on the topic "060802 Animal Cell and Molecular Biology"

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From gene to animal: An introduction to the molecular biology of animal development. Cambridge [Cambridgeshire]: Cambridge University Press, 1985.

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From gene to animal: An introduction to the molecular biology of animal development. 2nd ed. Cambridge [England]: Cambridge University Press, 1990.

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Rőszer, Tamás. The Biology of Subcellular Nitric Oxide. Dordrecht: Springer Netherlands, 2012.

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Pollard, Jeffrey W., and John M. Walker, eds. Animal Cell Culture (Methods in Molecular Biology Vol 5). Humana Press, 1990.

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McLaren, Anne, and Roger A. Pederson. Animal Applications of Research in Mammalian Development (Current Communications in Cell & Molecular Biology, Vol 4) (Current Communications in Cell and Molecular Biology). Cold Spring Harbor Laboratory Press, 1991.

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Organization and assembly of plant and animal extracellular matrix. San Diego: Academic Press, 1990.

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Turksen, Kursad. Embryonic Stem Cell Protocols: Volume II: Differentiation Models (Methods in Molecular Biology). 2nd ed. Humana Press, 2006.

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Heiser, William C. Gene Delivery to Mammalian Cells: Nonviral Gene Transfer Techniques (Methods in Molecular Biology) (Methods in Molecular Biology). Humana Press, 2003.

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Turksen, Kursad. Embryonic Stem Cell Protocols: Volume I: Isolation and Characterization (Methods in Molecular Biology). 2nd ed. Humana Press, 2006.

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Rőszer, Tamás. The Biology of Subcellular Nitric Oxide. Springer, 2014.

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Book chapters on the topic "060802 Animal Cell and Molecular Biology"

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Weissmann, C. "Molecular Biology of Prion Diseases." In Animal Cell Technology, 3–6. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5404-8_1.

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Okumoto, Kanji, and Yukio Fujiki. "Generation of Peroxisome-Deficient Somatic Animal Cell Mutants." In Methods in Molecular Biology, 319–27. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6937-1_29.

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Kang, Yibin. "Analysis of Cancer Stem Cell Metastasis in Xenograft Animal Models." In Methods in Molecular Biology, 7–19. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-280-9_2.

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Takakura, Hideo, Mitsuru Hattori, Miho Tanaka, and Takeaki Ozawa. "Cell-Based Assays and Animal Models for GPCR Drug Screening." In Methods in Molecular Biology, 257–70. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2336-6_18.

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Risal, Sanjiv, Deepak Adhikari, and Kui Liu. "Animal Models for Studying the In Vivo Functions of Cell Cycle CDKs." In Methods in Molecular Biology, 155–66. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2926-9_13.

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King, Rebecca M., and Victoria Korolik. "Characterization of Ligand–Receptor Interactions: Chemotaxis, Biofilm, Cell Culture Assays, and Animal Model Methodologies." In Methods in Molecular Biology, 149–61. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6536-6_13.

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Manella, Francis J. "“The FDA Quality/Compliance Continuum… Where do Cell Culture and Molecular Biology Products Stand”." In Animal Cell Technology: Basic & Applied Aspects, 529–35. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0848-5_81.

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Buzgariu, Wanda, Jean-Pierre Aubry-Lachainaye, and Brigitte Galliot. "Studying Stem Cell Biology in Intact and Whole-Body Regenerating Hydra by Flow Cytometry." In Methods in Molecular Biology, 373–98. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2172-1_20.

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AbstractThe freshwater Hydra polyp is a versatile model to study whole-body regeneration from a developmental as well as a cellular point of view. The outstanding regenerative capacities of Hydra are based on its three populations of adult stem cells located in the central body column of the animal. There, these three populations, gastrodermal epithelial, epidermal epithelial, and interstitial, continuously cycle in homeostatic conditions, and their activity is locally regulated after mid-gastric bisection. Moreover, they present an unusual cycling behavior with a short G1 phase and a pausing in G2. This particular cell cycle has been studied for a long time with classical microscopic methods. We describe here two flow cytometry methods that provide accurate and reproducible quantitative data to monitor cell cycle regulation in homeostatic and regenerative contexts. We also present a cell sorting procedure based on flow cytometry, whereby stem cells expressing a fluorescent reporter protein in transgenic lines can be enriched for use in applications such as transcriptomic, proteomic, or cell cycle analysis.
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Mito, Akiko, Kaori Kumazawa-Inoue, and Kyoko Kojima-Aikawa. "ZG16p, an Animal Homologue of Plant β-Prism Fold Lectins: Purification Methods of Natural and Recombinant ZG16p and Inhibition Assay of Cancer Cell Growth Using ZG16p." In Methods in Molecular Biology, 339–47. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0430-4_33.

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Milán-Rois, Paula, Ciro Rodriguez-Diaz, Milagros Castellanos, and Álvaro Somoza. "Conjugation of Nucleic Acids and Drugs to Gold Nanoparticles." In Methods in Molecular Biology, 103–16. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_6.

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AbstractGold nanoparticles (AuNPs) can be used as carriers for biomolecules or drugs in cell culture and animal models. Particularly, AuNPs ease their internalization into the cell and prevent their degradation. In addition, engineered AuNPs can be employed as sensors of a variety of biomarkers, where the electronic and optical properties of the AuNPs are exploited for a convenient, easy, and fast read out. However, in all these applications, a key step requires the conjugation of the different molecules to the nanoparticles. The most common approach exploits the great affinity of sulfur for gold. Herein, we summarize the methods used by our group for the conjugation of different molecules with AuNPs. The procedure is easy and takes around 2 days, where the reagents are slowly added, following an incubation at room temperature to ensure the complete conjugation. Finally, the unbound material is removed by centrifugation.
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Reports on the topic "060802 Animal Cell and Molecular Biology"

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Kang, Jing, Jun Zhang, Zongsheng Tian, Ye Xu, Jiangbi Li, and Mingxina Li. The efficacy and safety of immune-checkpoint inhibitor plus chemotherapy versus chemotherapy for non-small cell lung cancer: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0156.

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Review question / Objective: Population: histologically confirmed advanced NSCLC patients; Intervention: received immune-checkpoint inhibitor plus chemotherapy; Comparison:received chemotherapy; Outcome: reported OS, PFS, ORR and TRAEs; Study design: RCT. Condition being studied: Lung cancer is the primary cause of cancer-related deaths, with an estimated 2.20 million new cases and 1.79 million deaths every year, and 85% of all primary lung cancers are non-small cell lung cancer. Eligibility criteria: Studies were considered eligible if they met the following criteria: (1) being an randomized controlled trial published in English, (2) histologically confirmed advanced NSCLC patients, (3) reported OS, PFS, ORR and TRAEs, (4) the intervention group received immune-checkpoint inhibitor plus chemotherapy, while the control group received chemotherapy, (5) When numerous papers reporting the same trial were found, the most current or most complete publications were chosen. The following were the exclusion criteria: (1) duplicate articles, (2) reviews, meta-analyses, case reports, editorials and letters, (3) molecular biology or animal research, (4) retrospective or prospective observational cohort studies.
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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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