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Academic literature on the topic 'Palladin'

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Published: 9 March 2023
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Journal articles on the topic "Palladin"

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Mayer, Ori, Joshua Bugis, Daria Kozlova, Aviv Leemann, Shahar Mansur, Ilan Peerutin, Noga Mendelovich, Meital Mazin, Dinorah Friedmann-Morvinski, and Noam Shomron. "Cytoskeletal Protein Palladin in Adult Gliomas Predicts Disease Incidence, Progression, and Prognosis." Cancers 14, no. 20 (October 19, 2022): 5130. http://dx.doi.org/10.3390/cancers14205130.

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Brain tumors comprise over 100 types of masses, differing in the following: location; patient age; molecular, histological, and immunohistochemical characteristics; and prognosis and treatment. Glioma tumors originate from neuroglia, cells supporting the brain. Palladin, a structural protein widely expressed in mammalian tissues, has a pivotal role in cytoskeletal dynamics and motility in health and disease. Palladin is linked to the progression of breast, pancreatic, and renal cancers. In the central nervous system, palladin is involved in embryonic development, neuronal maturation, the cell cycle, differentiation, and apoptosis. However, the role of palladin in brain tumors is unknown. In this work, we explored palladin’s role in glioma. We analyzed clinical data, along with bulk and single-cell gene expression. We then validated our results using IHC staining of tumor samples, together with qRT-PCR of glioma cell lines. We determined that wild-type palladin-4 is overexpressed in adult gliomas and is correlated with a decrease in survival. Palladin expression outperformed clinically used prognostic markers and was most prominent in glioblastoma. Finally, we showed that palladin originates from the malignant cell population. Our findings indicate that palladin expression might be linked to adult glioma progression and is associated with prognosis.
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Sun, Haimin, Xinlei Chen, Xin Xu, and Sai-juan Chen. "Palladin Plays an Important Role in Pulmonary Cellular Infiltration in Differentiation Syndrome." Blood 124, no. 21 (December 6, 2014): 4947. http://dx.doi.org/10.1182/blood.v124.21.4947.4947.

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Abstract Background Acute promyelocytic leukemia (APL) is characterized by a specific t(15;17) chromosomal translocation, which fuses the promyelocytic leukemia (PML) gene on chromosome 15 to the retinoic acid receptor-(RARα ) gene on chromosome 17. The introduction of all-trans retinoic acid (ATRA) into the treatment strategy of APL fundamentally changed the management and outcome of this disease. Treatment with ATRA relieves this blockage, resulting in terminal differentiation of the APL blasts. Aims To investigate the molecular mechanisms of ATRA induced differentiation, we have described a series of novel genes up-regulated by ATRA. One of them, Rig-K (Retinoic-acid-induced gene-K), was the human homolog of palladin. This study is mainly focus on the function of palladin gene during the process of differentiation. Methods 1. Lentivirus shRNA expression system was used to generate stable palladin konckdown NB4 cell lines. Cells morphological and the expression of differentiation markers were observed； 2. Use flow cytometry and immunofluorescence to compare the difference of cell cycle, cell proliferation, apoptosis, cell migration and granulocyte related functions such as adhesion, phagocytosis between control and palladin knockdown group; 3. Real-time PCR and chemokines antibody array were used to detect the effect of palladin reduction on the levels of chemokines secreted by NB4 cells； 4. Use microgravity rotary cell culture system to study the infiltration capacity of differentiated NB4 cells to lung tissues. Observe whether palladin knockdown play a role in this processes. Results 1. Palladin knockdown has minor effect on NB4 differentiation based on cell morphology and granulocytic differentiation-related antigens. Palladin knockdown can partly relieved the proliferation inhibition effect during differentiation. Cycle arrest can partly relieved by palladin knock down manifest as reduced G0/G1 arrest. Palladin knock down can also remarkable reduce apoptosis rate compared with control group at 96 hours time point; 2. The phagocytosis level was about 50% dropped when the palladin was knocked down, suggest palladin play important roles in phagocytosis progress. Besides, we also observed the localization of palladin in the phagocytic cup, and palladin is colocalizated with F-actin in phagocytic cup. The migration level was also about 50% dropped when the palladin was knocked down in differentiated NB4 cells. Palladin colocalization with F-actin and vinculin, knockdown of palladin alter the distribution of F-actin and vinculin, suggest palladin take part in the formation of actin related structures; 3. Differentiation induction of APL cells is associated with increased expression of specific adhesion molecules and inflammatory cytokines, palladin knockdown decrease the upregulation of many chemokines; 4. Palladin knockdown also reduced infiltration ability of differentiated NB4 cells into lung tissues. Conclusion Palladin knockdown significantly decreased the granulocyte related function of differentiated APL cells, especially cell motile ability and secretion of chemokines. In vitro model shows that palladin knockdown can inhibit the invasion ability of differentiated APL cells into lung tissues, suggest palladin may play important roles in retinoic acid syndrome. Disclosures No relevant conflicts of interest to declare.
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Sun, Haimin, Xinlei Chen, Jiang Zhu, Zhu Chen, and Saijuan Chen. "Palladin Regulates Receptor Clustering and Actin Dynamics in Phagocytosis." Blood 128, no. 22 (December 2, 2016): 2505. http://dx.doi.org/10.1182/blood.v128.22.2505.2505.

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Abstract BACKGROUND: Palladin is an actin microfilament associated protein, which together with myotilin and myopalladin form a novel cytoskeletal IgC2 domain protein family. However, little is known about the function of Palladin in myeloid cells. Here, we focus on the function of Palladin in phagocytosis. METHODS: We used ATRA induced differentiated NB4 cells as neutrophil-like cells, and lenti-viruses were used to build cell lines with palladin or ocrl knockdown and VAMP3-mcherry overexpression. Flow cytometry and immunofluorescence were used to detect the phagocytic ability under conditional opsonins, and the role of palladin knockdown on phagocytic events and F-actin dynamics were observed. CD32 antibodies followed with fluorescent secondary antibody were used as immune complex to stimulate FcγR clustering. We performed the mass spectrometry analysis on the immunoprecipitation (IP) lysate of differentiated NB4 cells, and the protein-protein interactions were confirmed by co-IP experiments; the colocalization and recruitment of different proteins or moleculars were observed under microscopy. RESULTS: Palladin was up-regulated during ATRA induced differentiation of several AML cell lines, as well as primary mouse bone marrow cells, and its upregulation correlated with increased phagocytic ability. Palladin defective cells showed impaired serum-mediated, IgG- or complement-mediated phagocytosis. The binding ability was measured at 4℃. After 1 hour incubation, ~17% of control cells bound with beads, whereas only ~7% palladin knockdown cells bound with beads, which suggests that Palladin regulated the particle binding. Using serum-opsonized zymosan-FITC as phagocytic targets, we found early phagosome formation, including the pseudopod extension and phagosome closure, was impaired in palladin knockdown cells. However, no significant effect was observed on the recruitment of VAMP3-mcherry, EEA1, Rab7 and LAMP1, so Palladin may not affect the focal exocytosis and phagosome maturation. The binding defect in Palladin-deficient cells was not attributable to difference in the cell surface expression of Fcγ receptor (FcγR). However, the FcγR clustering was much lower in Palladin-deficient cells. We explored how Palladin influenced the FcγR clustering, and our results showed that Palladin could regulate actin cytoskeleton dynamics and c-Src kinase activation, which resulted in the FcγR clustering. We also found that in palladin knockdown cells the actin remodeling was detained at both pseudopod extension stage and actin deploymerization stage. The Rac1 were accumulated in higher amount in the blocked cups formed in palladin KD cells, while no significant difference in Cdc42 recruitment. The recruitment intensity of Apr3 was higher in control cells than palladin KD cells. These results suggested that Palladin participated in the actin dynamics during phagocytic cup formation. We found OCRL is a new Palladin-interacted protein. Palladin interacted with OCRL's 5PPase domain through its third IgC2 domain. Palladin depletion caused a decrease of ~30% OCRL recruitment, retention of PI(4,5)P2, as well as more F-actin at phagosome. These observation suggested that Palladin regulated the recruitment of OCRL at sites of phagosome, and might play an essential role in regulating the hydrolysis of PI(4,5)P2, actin depolymerization and the completion of phagosome closure. CONCLUSIONS: We identify the role of Palladin in phagocytic receptor clustering and Palladin as an early coordinator in actin dynamics during phagosome formation in myeloid cells. Disclosures No relevant conflicts of interest to declare.
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Parast, Mana M., and Carol A. Otey. "Characterization of Palladin, a Novel Protein Localized to Stress Fibers and Cell Adhesions." Journal of Cell Biology 150, no. 3 (August 7, 2000): 643–56. http://dx.doi.org/10.1083/jcb.150.3.643.

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Here, we describe the identification of a novel phosphoprotein named palladin, which colocalizes with α-actinin in the stress fibers, focal adhesions, cell–cell junctions, and embryonic Z-lines. Palladin is expressed as a 90–92-kD doublet in fibroblasts and coimmunoprecipitates in a complex with α-actinin in fibroblast lysates. A cDNA encoding palladin was isolated by screening a mouse embryo library with mAbs. Palladin has a proline-rich region in the NH2-terminal half of the molecule and three tandem Ig C2 domains in the COOH-terminal half. In Northern and Western blots of chick and mouse tissues, multiple isoforms of palladin were detected. Palladin expression is ubiquitous in embryonic tissues, and is downregulated in certain adult tissues in the mouse. To probe the function of palladin in cultured cells, the Rcho-1 trophoblast model was used. Palladin expression was observed to increase in Rcho-1 cells when they began to assemble stress fibers. Antisense constructs were used to attenuate expression of palladin in Rcho-1 cells and fibroblasts, and disruption of the cytoskeleton was observed in both cell types. At longer times after antisense treatment, fibroblasts became fully rounded. These results suggest that palladin is required for the normal organization of the actin cytoskeleton and focal adhesions.
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Mykkänen, Olli-Matti, Mikaela Grönholm, Mikko Rönty, Maciej Lalowski, Paula Salmikangas, Heli Suila, and Olli Carpén. "Characterization of Human Palladin, a Microfilament-associated Protein." Molecular Biology of the Cell 12, no. 10 (October 2001): 3060–73. http://dx.doi.org/10.1091/mbc.12.10.3060.

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Actin-containing microfilaments control cell shape, adhesion, and contraction. In striated muscle, α-actinin and other Z-disk proteins coordinate the organization and functions of actin filaments. In smooth muscle and nonmuscle cells, periodic structures termed dense bodies and dense regions, respectively, are thought to serve functions analogous to Z-discs. We describe here identification and characterization of human palladin, a protein expressed mainly in smooth muscle and nonmuscle and distributed along microfilaments in a periodic manner consistent with dense regions/bodies. Palladin contains three Ig-domains most homologous to the sarcomeric Z-disk protein myotilin. The N terminus includes an FPPPP motif recognized by the Ena-Vasp homology domain 1 domain in Ena/vasodilatator-stimulated phosphoprotein (VASP)/Wiscott-Aldrich syndrome protein (WASP) protein family. Cytoskeletal proteins with FPPPP motif target Ena/VASP/WASP proteins to sites of actin modulation. We identified palladin in a yeast two-hybrid search as an ezrin-associated protein. An interaction between palladin and ezrin was further verified by affinity precipitation and blot overlay assays. The interaction was mediated by the α-helical domain of ezrin and by Ig-domains 2–3 of palladin. Ezrin is typically a component of the cortical cytoskeleton, but in smooth muscle cells it is localized along microfilaments. These cells express palladin abundantly and thus palladin may be involved in the microfilament localization of ezrin. Palladin expression was up-regulated in differentiating dendritic cells (DCs), coinciding with major cytoskeletal and morphological alterations. In immature DCs, palladin localized in actin-containing podosomes and in mature DCs along actin filaments. The regulated expression and localization suggest a role for palladin in the assembly of DC cytoskeleton.
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Boukhelifa, Malika, Mana M. Parast, Juli G. Valtschanoff, Anthony S. LaMantia, Rick B. Meeker, and Carol A. Otey. "A Role for the Cytoskeleton-associated Protein Palladin in Neurite Outgrowth." Molecular Biology of the Cell 12, no. 9 (September 2001): 2721–29. http://dx.doi.org/10.1091/mbc.12.9.2721.

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The outgrowth of neurites is a critical step in neuronal maturation, and it is well established that the actin cytoskeleton is involved in this process. Investigators from our laboratory recently described a novel protein named palladin, which has been shown to play an essential role in organizing the actin cytoskeleton in cultured fibroblasts. We investigated the expression of palladin in the developing rat brain by Western blot and found that the E18 brain contained a unique variant of palladin that is significantly smaller (∼85 kDa) than the common form found in other developing tissues (90–92 kDa). Because the expression of a tissue-specific isoform suggests the possibility of a cell type-specific function, we investigated the localization and function of palladin in cultured cortical neurons. Palladin was found preferentially targeted to the developing axon but not the dendrites and was strongly localized to the axonal growth cone. When palladin expression was attenuated by transfection with antisense constructs in both the B35 neuroblastoma cell line and in primary cortical neurons, a reduction in the expression of palladin resulted in a failure of neurite outgrowth. These results implicate palladin as a critical component of the developing nervous system, with an important role in axonal extension.
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Wall, Michelle E., Andrew Rachlin, Carol A. Otey, and Elizabeth G. Loboa. "Human adipose-derived adult stem cells upregulate palladin during osteogenesis and in response to cyclic tensile strain." American Journal of Physiology-Cell Physiology 293, no. 5 (November 2007): C1532—C1538. http://dx.doi.org/10.1152/ajpcell.00065.2007.

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Cell morphology may be an important stimulus during differentiation of human adipose-derived adult stem (hADAS) cells, but there are limited studies that have investigated the role of the cytoskeleton or associated proteins in hADAS cells undergoing differentiation. Palladin is an actin-associated protein that plays an integral role in focal adhesion and cytoskeleton organization. In this study we show that palladin was expressed by hADAS cells and was modulated during osteogenic differentiation and in response to cyclic tensile strain. Human ADAS cells expressed the 90- and 140-kDa palladin isoforms and upregulated expression of both isoforms after culture in conditions that promoted osteogenesis. Palladin mRNA expression levels were also increased in hADAS cells subjected to cyclic tensile strain. Knockdown of the palladin gene during osteogenesis resulted in decreased actin stress fibers and decreased protein levels of Eps8, an epidermal growth factor receptor tyrosine kinase that colocalizes with actin. Silencing the palladin gene, however, did not affect hADAS cells' commitment down the osteogenic lineage.
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Artelt, Nadine, Tim A. Ludwig, Henrik Rogge, Panagiotis Kavvadas, Florian Siegerist, Antje Blumenthal, Jens van den Brandt, et al. "The Role of Palladin in Podocytes." Journal of the American Society of Nephrology 29, no. 6 (May 2, 2018): 1662–78. http://dx.doi.org/10.1681/asn.2017091039.

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Background Podocyte loss and effacement of interdigitating podocyte foot processes are the major cause of a leaky filtration barrier and ESRD. Because the complex three-dimensional morphology of podocytes depends on the actin cytoskeleton, we studied the role in podocytes of the actin bundling protein palladin, which is highly expressed therein.Methods We knocked down palladin in cultured podocytes by siRNA transfection or in zebrafish embryos by morpholino injection and studied the effects by immunofluorescence and live imaging. We also investigated kidneys of mice with podocyte-specific knockout of palladin (PodoPalld−/− mice) by immunofluorescence and ultrastructural analysis and kidney biopsy specimens from patients by immunostaining for palladin.Results Compared with control-treated podocytes, palladin-knockdown podocytes had reduced actin filament staining, smaller focal adhesions, and downregulation of the podocyte-specific proteins synaptopodin and α-actinin-4. Furthermore, palladin-knockdown podocytes were more susceptible to disruption of the actin cytoskeleton with cytochalasin D, latrunculin A, or jasplakinolide and showed altered migration dynamics. In zebrafish embryos, palladin knockdown compromised the morphology and dynamics of epithelial cells at an early developmental stage. Compared with PodoPalld+/+ controls, PodoPalld−/− mice developed glomeruli with a disturbed morphology, an enlarged subpodocyte space, mild effacement, and significantly reduced expression of nephrin and vinculin. Furthermore, nephrotoxic serum injection led to significantly higher levels of proteinuria in PodoPalld−/− mice than in controls. Kidney biopsy specimens from patients with diabetic nephropathy and FSGS showed downregulation of palladin in podocytes as well.Conclusions Palladin has an important role in podocyte function in vitro and in vivo.
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Gurung, Ritu, Rahul Yadav, Joseph G. Brungardt, Albina Orlova, Edward H. Egelman, and Moriah R. Beck. "Actin polymerization is stimulated by actin cross-linking protein palladin." Biochemical Journal 473, no. 4 (February 9, 2016): 383–96. http://dx.doi.org/10.1042/bj20151050.

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Our results indicate palladin stimulates actin polymerization by accelerating the nucleation step, while also enhancing filament stability and altering filament architecture. Palladin regulates a distinct actin nucleation mechanism that may underlie the assembly of actin in invasive cell motility.
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Artelt, Nadine, Alina M. Ritter, Linda Leitermann, Felix Kliewe, Rabea Schlüter, Stefan Simm, Jens van den Brandt, Karlhans Endlich, and Nicole Endlich. "The podocyte-specific knockout of palladin in mice with a 129 genetic background affects podocyte morphology and the expression of palladin interacting proteins." PLOS ONE 16, no. 12 (December 8, 2021): e0260878. http://dx.doi.org/10.1371/journal.pone.0260878.

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Proper and size selective blood filtration in the kidney depends on an intact morphology of podocyte foot processes. Effacement of interdigitating podocyte foot processes in the glomeruli causes a leaky filtration barrier resulting in proteinuria followed by the development of chronic kidney diseases. Since the function of the filtration barrier is depending on a proper actin cytoskeleton, we studied the role of the important actin-binding protein palladin for podocyte morphology. Podocyte-specific palladin knockout mice on a C57BL/6 genetic background (PodoPalldBL/6-/-) were back crossed to a 129 genetic background (PodoPalld129-/-) which is known to be more sensitive to kidney damage. Then we analyzed the morphological changes of glomeruli and podocytes as well as the expression of the palladin-binding partners Pdlim2, Lasp-1, Amotl1, ezrin and VASP in 6 and 12 months old mice. PodoPalld129-/- mice in 6 and 12 months showed a marked dilatation of the glomerular tuft and a reduced expression of the mesangial marker protein integrin α8 compared to controls of the same age. Furthermore, ultrastructural analysis showed significantly more podocytes with morphological deviations like an enlarged sub-podocyte space and regions with close contact to parietal epithelial cells. Moreover, PodoPalld129-/- of both age showed a severe effacement of podocyte foot processes, a significantly reduced expression of pLasp-1 and Pdlim2, and significantly reduced mRNA expression of Pdlim2 and VASP, three palladin-interacting proteins. Taken together, the results show that palladin is essential for proper podocyte morphology in mice with a 129 background.
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Dissertations / Theses on the topic "Palladin"

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Stack, Christianna Otey Carol A. "The role of palladin in pancreatic cancer." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2072.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Feb. 17, 2009). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Cell and Molecular Physiology." Discipline: Cell and Molecular Physiology; Department/School: Medicine.
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Ludwig, Tim Alexander [Verfasser]. "Der Zebrafisch als Modellorganismus für den Knockdown von Palladin / Tim Alexander Ludwig." Greifswald : Universitätsbibliothek Greifswald, 2014. http://d-nb.info/1059782014/34.

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Kim, Pil-Sang [Verfasser]. "Bedeutung von Palladin für die trainingsinduzierte Anpassung der Skelettmuskulatur / Pil-Sang Kim." Köln : Deutsche Sporthochschule Köln, 2012. http://d-nb.info/1070867489/34.

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Arneman, Daniel Kenneth Anton Eva S. "The role of palladin in actin organization implications for the glial scar /." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1612.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Cell and Molecular Physiology." Discipline: Cell and Molecular Physiology; Department/School: Medicine.
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Brungardt, Joseph G. "The phosphorylation of palladin and the effect on its interaction with actin binding, bundling, and polymerization." Diss., Wichita State University, 2013. http://hdl.handle.net/10057/6421.

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Metastatic cell motility, namely breast cancer, has been shown to be regulated in part by the protein palladin. Palladin is a recently described actin binding and bundling protein whose expression level is related to metastatic cancer cell motility. Palladin plays a role in the regulation of actin, a highly abundant protein within a cell, which acts as a cell’s skeleton. Actin is also the structural basis of invasive cellular structures known as invadopodia, which cross the extracellular matrix and allow cells to invade surrounding tissue structures. Palladin has been shown to regulate actin bundles within these invasive structures. Further studies have shown that Akt1, a prominent and highly studied protein kinase, phosphorylates palladin at a linker region between its immunoglobulin domains that are critical for actin bundling. Our work builds upon initial cell-based assays which show that normal cell function is altered when phosphorylation of palladin is misregulated. We utilized biochemical assays to quantify how phosphorylation of palladin affects the structure and function of actin to further understand both of their roles in cancer cell motility.
Thesis (Ph.D.)--Wichita State University, College of Liberal Arts and Sciences, Dept. of Chemistry
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MASTROTOTARO, GIUSEPPINA. "Molecular characterization of the sarcomeric Z-line proteins nebulette and palladin in the heart: roles in cardiac structure, function, and disease." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/94177.

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The sarcomeres are the smallest contractile units of striated muscle. It is formed by actin (thin) and myosin (thick) filaments that slide over each other during contraction and is stabilized by titin filaments, which acts as a spring during contraction. In the Z-line at the boundary between sarcomeres, actin and titin filaments are cross-linked and the contractile apparatus is connected with the cytoskeleton and extracellular matrix. The Z-line is important for efficient force generation and maintenance of cardiac structure, and is a focal point for mechanosensing and signal transduction. Consistently, mutations in many Z-line associated proteins have been associated with cardiomyopathies, including nebulette and its interaction partner myopalladin. On the other hand, the role of palladin (PALLD), a homologue of myopalladin (MYPN) associated with nebulette, in the heart has remained unknown. The aim of the present project was to investigate the function of nebulette and palladin in the heart. Nebulette is a 109 kDa modular protein composed of nebulin repeats and a C-terminal SH3 domain. In vitro studies have suggested a role of nebulette in stabilizing the thin filament, and missense mutations in the nebulette gene have been found to be causative for dilated cardiomyopathy and endocardial fibroelastosis in human and mice. However, the role of nebulette in vivo has remained unknown. To study the functional role of nebulette in the heart in vivo, we generated and studied nebulette knockout (nebl-/-) mice. Functional analyses revealed normal cardiac function of nebl-/- mice both at basal conditions and in response to transaortic constriction (TAC). Furthermore, histological, immunofluorescence, and Western blot analyses showed no cardiac abnormalities in nebl-/- mice. On the other hand, Z-line widening was observed from 5 months of age and the presence of chronic cardiac stress was suggested by the upregulation of cardiac stress responsive genes. Thus, nebulette may play an important role for Z-line integrity, while the absence of a functional phenotype of nebl-/- mice suggests that nebulette cardiomyopathy mutations have gain-of-function effects. PALLD, MYPN, and myotilin (MYOT) make up a small protein family of immunoglobulin-containing proteins in the sarcomeric Z-line associated with α-actinin and filamentous actin. MYPN and MYOT are expressed as single isoforms in striated muscle, while PALLD is ubiquitously expressed in several isoforms. The longest 200 kDa PALLD isoform is expressed predominantly in striated muscle and is highly homologous in structure to MYPN, suggesting a similar role of the two proteins in striated muscle. However, while mutations in the MYPN gene have been associated with dilated, hypertrophic, and restrictive cardiomyopathy, the role of PALLD in the heart has remained unknown. Since PALLD knockout mice are embryonic lethal, to study the role of PALLD in heart, we generated constitutive (cPKO) and inducible (cPKOi) cardiac specific PALLD knockout mice. cPKO mice showed normal cardiac function both at basal conditions and following TAC, while inducible knockout of PALLD in adult cPKOi mice resulted in progressive cardiac dilation and systolic dysfunction, associated with fibrosis, upregulation of markers of cardiac pathological remodeling, and ERK activation. Furthermore, PALLD was found to activate serum response factor (SRF) signaling and strongly increase MRTF-A-mediated activation of SRF, likely through its direct interaction MRTF-A and role in modulating actin dynamics. The development of a dilated cardiomyopathy in cPKOi mice induced at adult stage demonstrates that PALLD is essential for normal cardiac function and suggests that PALLD gene mutations may be causative for cardiomyopathy. The absence of a cardiac phenotype of cPKO mice may be due to compensatory mechanisms.
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Artelt, Nadine Verfasser], Karlhans [Akademischer Betreuer] Endlich, Karlhans [Gutachter] Endlich, Thomas [Gutachter] Weide, and Sigrid [Gutachter] [Hoffmann. "Untersuchung des Einflusses von Palladin auf das Aktinzytoskelett von Podozyten / Nadine Artelt ; Gutachter: Karlhans Endlich, Thomas Weide, Sigrid Hoffmann ; Betreuer: Karlhans Endlich." Greifswald : Universität Greifswald, 2020. http://d-nb.info/1207502073/34.

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Artelt, Nadine Verfasser], Karlhans [Akademischer Betreuer] [Endlich, Karlhans Gutachter] Endlich, Thomas [Gutachter] [Weide, and Sigrid [Gutachter] Hoffmann. "Untersuchung des Einflusses von Palladin auf das Aktinzytoskelett von Podozyten / Nadine Artelt ; Gutachter: Karlhans Endlich, Thomas Weide, Sigrid Hoffmann ; Betreuer: Karlhans Endlich." Greifswald : Universität Greifswald, 2020. http://d-nb.info/1207502073/34.

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Artelt, Nadine [Verfasser], Karlhans [Akademischer Betreuer] Endlich, Karlhans [Gutachter] Endlich, Thomas [Gutachter] Weide, and Sigrid [Gutachter] Hoffmann. "Untersuchung des Einflusses von Palladin auf das Aktinzytoskelett von Podozyten / Nadine Artelt ; Gutachter: Karlhans Endlich, Thomas Weide, Sigrid Hoffmann ; Betreuer: Karlhans Endlich." Greifswald : Universität Greifswald, 2020. http://d-nb.info/1207502073/34.

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Frizzale, Tommaso. "Palladio digitale. Studio e ricostruzione di un progetto palladiano : villa Mocenigo." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amslaurea.unibo.it/2132/.

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L’obiettivo che l’elaborato si prefigge consiste nel dar forma ad un progetto palladiano rimasto sulla carta attraverso l’utilizzo delle tecnologie informatiche. Nello specifico si è ricostruita Villa Mocenigo in forma tridimensionale attraverso uno schizzo del progetto fatto su carta dallo stesso Palladio nel 1550. Lo schizzo della pianta, conservato al RIBA di Londra, anticiperebbe il successivo progetto finale pubblicato ne “I Quattro Libri dell’Architettura” ma rimasto comunque incompiuta. Il linguaggio di base utilizzato per la definizione dell’ipotesi progettuale del modello 3D è stato attinto dalle regole generali di proporzionamento “alla maniera degli antichi” che lo stesso Architetto illustra nel suo trattato. Al fine di rendere l’ipotesi ricostruttiva il più possibile in linea con il metodo di proporzionamento palladiano, come esercitazione, si è partiti dallo studio preparatorio di un altro progetto: Villa Sarego, edificata solo in parte. A partire quindi dalla ricostruzione 3D basata sui disegni dei rilievi eseguiti dal CISAAP è stata avanzata l’ipotesi di ricostruzione totale della villa, completa della parte incompiuta. Lo studio sintetizzato in questo elaborato ha anche riguardato: la composizione architettonica e lo studio delle regole proporzionali evolutesi nel tempo; il processo di digitalizzazione e archiviazione delle opere palladiane e i progetti attualmente in corso; escursus storico sulle ville romane; le opera di Palladio, costruite e progettate.
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Books on the topic "Palladin"

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Poli͡akova, N. M. Aleksandr Vladimirovich Palladin: Dokumenty, fotografii. Kiev: Nauk. dumka, 1985.

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2

P, Strogonov B., ed. Vladimir Ivanovich Palladin, 1859-1922. Moskva: "Nauka", 1986.

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Athenaeum, Redwood Library and, and Newport Symposium (1996 : Newport, R.I.), eds. Vitruvius Americanus: Colonial Newport in the Palladin tradition. Newport, RI: The Library, 1996.

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Jörgen, Bracker, and Museum für Hamburgische Geschichte, eds. Bauen nach der Natur--Palladio: Die Erben Palladios in Nordeuropa. Ostfildern-Ruit: G. Hatje, 1997.

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Vasiliĭ, Uspenskiĭ, and Museo Correr, eds. Russia palladiana: Palladio e la Russia dal barocco al modernismo. Venezia: [publisher not identified], 2014.

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Palladio nel Colognese: La Cucca dei Serego : architettura palladiane, paesaggio ed arte. Rimini: Agenzia NFC, 2012.

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Palladio, Andrea. Palladio. London: Royal Academy of Arts, 2008.

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Palladio. London: Penguin Books, 1991.

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Ackerman, James S. Palladio. 3rd ed. London: Penguin Books, 2008.

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Palladio. Milano: Skira, 2008.

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Book chapters on the topic "Palladin"

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Constant, Caroline. "Einleitung." In Der Palladio-Führer, 1–18. Wiesbaden: Vieweg+Teubner Verlag, 1988. http://dx.doi.org/10.1007/978-3-322-84283-1_1.

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Constant, Caroline. "Die Bauten." In Der Palladio-Führer, 19–139. Wiesbaden: Vieweg+Teubner Verlag, 1988. http://dx.doi.org/10.1007/978-3-322-84283-1_2.

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Thies, Harmen H. "Palladio, Andrea." In Kindlers Literatur Lexikon (KLL), 1. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_16035-1.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Oxygen." In Pd Palladium, 1–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_1.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Boron." In Pd Palladium, 256–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_10.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Carbon." In Pd Palladium, 262–311. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_11.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Silicon." In Pd Palladium, 312–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_12.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Phosphorus." In Pd Palladium, 323–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_13.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Arsenic." In Pd Palladium, 343–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_14.

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Griffith, William P., Stephen D. Robinson, and Kurt Swars. "Palladium and Antimony." In Pd Palladium, 352. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-09188-3_15.

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Conference papers on the topic "Palladin"

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Goicoechea, SM, H. Prentice-Dunn, B. Bednarski, H. Kim, and CA Otey. "Palladin expression contributes to invasive motiliy in metastatic breast cancer cells." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6018.

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Gupta, Vivekanand, Jeffrey Simons, Daniel Bassi, Tahseen I. Al-Saleem, Robert G. Uzzo, and Edna Cukierman. "Abstract 3171: Stromal palladin is a poor prognostic marker in renal cell carcinoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3171.

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Brentnall, Teresa Averill, Lisa Lai, Mary Bronner, and Ru Chen. "Abstract B61: Arousal of cancer-associated stromal fibroblasts: Palladin-activated fibroblasts promote tumor invasion." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-b61.

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Gane, Daria Gomez. "Pythagorean Palladio: Palladian Proportionality Patterns Decoded?" In The 38th Annual Conference of the Society of Architectural Historians Australia and New Zealand. online: SAHANZ, 2022. http://dx.doi.org/10.55939/a4012pbk5w.

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Abstract:
There seem to be many understated assumptions in Palladio’s Four Books on Architecture. He tells us what to do, but never fully explains in detail how he gets to the recommended methods. For instance he uses drawings that understate the use of the root two rectangle (Figure V) in the first geometric method suggested to calculate the heights of vaults and uses the numbers of the tetraktys – without mentioning it - to “calculate” and provide an example of “harmonic” proportion. Had he only been a little more specific many misconceptions about his work – as being not entirely clear and somehow mysterious- might have never eventuated. In this brief work we show Palladio’s use in his designed and built work of one of his favourite proportions, the “proportione diagonea” already mentioned by Serlio, none other than the root two rectangle - the root two being, according to Wittkower, in his 1949 seminal work, the only irrational number of relevance in Renaissance architectural proportionality theory. A brief explanation of how the Tetraktys and Pythagorean Lambda were allegedly used by the stonemason turned architect to “calculate” “arithmetic”, “geometric” and “harmonic” means is provided.
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Alexander, Jennifer I., and Edna Cukierman. "Abstract 2979: Inhibition of palladin in cancer associated fibroblast impedes pancreatic ductal adenocarcinoma associated desmoplasia." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2979.

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Alexander, Jennifer, and Edna Cukierman. "Abstract B070: Loss of cytoskeletal protein palladin desensitizes pancreatic cancer associated fibroblast to TGFβ1-dependent desmoplastic induction." In Abstracts: Eleventh AACR Conference on The Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 2-5, 2018; New Orleans, LA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7755.disp18-b070.

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Owen, Meredith, Michael Kerber, Silvia Goicoechea, Rosa F. Hwang, Hong Jin Kim, and Carol A. Otey. "Abstract B46: The actin-binding protein palladin localizes to the nucleus of pancreatic tumor-associated fibroblasts and regulates gene expression." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-b46.

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Cappello, Nora. "Palladio e Roma." In Encontro da História da Arte. Universidade Estadual de Campinas, 2007. http://dx.doi.org/10.20396/eha.3.2007.4199.

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Benros, Deborah, Jose Pinto Duarte, and Sean Hanna. "An alternative Palladian shape grammar: A subdivision grammar for Palladian villas." In CAADRIA 2012: Beyond Codes and Pixels. CAADRIA, 2012. http://dx.doi.org/10.52842/conf.caadria.2012.415.

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Becker, Steffen. "The palladio component model." In the first joint WOSP/SIPEW international conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1712605.1712651.

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Reports on the topic "Palladin"

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Berman, Morris, and David Gray. XM982 Palladin Hold Down Strap Characterization. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada479579.

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Peters, John, Jay McCloskey, Trevor Douglas, Mark Young, Stuart Snyder, and Brian Gurney. MONTANA PALLADIUM RESEARCH INITIATIVE. Office of Scientific and Technical Information (OSTI), May 2012. http://dx.doi.org/10.2172/1039692.

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Burns, Jon D. Californium Recovery from Palladium Wire. Office of Scientific and Technical Information (OSTI), August 2014. http://dx.doi.org/10.2172/1185525.

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Pfefferle, L. D., and A. Datye. Palladium Catalysis for Energy Applications. Office of Scientific and Technical Information (OSTI), March 2001. http://dx.doi.org/10.2172/833766.

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Pfefferle, L. D., and Abhaya Datye. Palladium catalysis for energy applications. Office of Scientific and Technical Information (OSTI), March 2001. http://dx.doi.org/10.2172/799205.

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Papaconstantopoulos, Dimitrios. Highly Concentrated Palladium Hydrides/Deuterides; Theory. Office of Scientific and Technical Information (OSTI), November 2013. http://dx.doi.org/10.2172/1116995.

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Zaczek, Christoph. Electrolysis of Palladium in Heavy Water. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6927.

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Flanagan, T. B. Pressure-composition-isotherms of palladium alloys. Office of Scientific and Technical Information (OSTI), November 1996. http://dx.doi.org/10.2172/758823.

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Silver, G., B. Leahy, and F. Martin. Preparation and characterization of palladium particles. Office of Scientific and Technical Information (OSTI), February 1989. http://dx.doi.org/10.2172/6505358.

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Tuggle, D. G., T. N. Claytor, and S. F. Taylor. Tritium evolution from various morphologies of palladium. Office of Scientific and Technical Information (OSTI), April 1994. http://dx.doi.org/10.2172/10138236.

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