Relevant bibliographies by topics / P38a

Academic literature on the topic 'P38a'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'P38a.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "P38a"

1

Hale, Karin K., David Trollinger, Marynette Rihanek, and Carl L. Manthey. "Differential Expression and Activation of p38 Mitogen-Activated Protein Kinase α, β, γ, and δ in Inflammatory Cell Lineages." Journal of Immunology 162, no. 7 (April 1, 1999): 4246–52. http://dx.doi.org/10.4049/jimmunol.162.7.4246.

Full text
Abstract:
Abstract Four p38 mitogen-activated protein kinases (p38α, β, γ, δ) have been described. To understand the role of p38 family members in inflammation, we determined their relative expression in cells that participate in the inflammatory process. Expression was measured at the level of mRNA by reverse-transcriptase PCR and protein by Western blot analysis. p38α was the dominant form of p38 in monocytes; expression of p38δ was low and p38β was undetected. In macrophages, p38α and p38δ were abundant, but p38β was undetected. p38α and p38δ were also expressed by neutrophils, CD4+ T cells, and endothelial cells. Again, p38β was not detected in neutrophils, although low amounts were present in CD4+ T cells. In contrast, p38β was abundant in endothelial cells. p38γ protein was not detected in any cell type, although p38γ mRNA was present in endothelial cells. Immunokinase assays showed a strong activation of p38α and a lesser activation of p38δ in LPS-stimulated macrophages. Abs specific for mono- and dual-phophorylated forms of p38 suggested that LPS induces dual phosphorylation of p38α, but primarily mono-phosphorylation of p38δ. IL-1β activated p38α and p38β in endothelial cells. However, p38α was the more activated form based on kinase assays and phosphorylation analysis. Expression and activation patterns of p38α in macrophages and endothelial cells suggest that p38α plays a major role in the inflammatory response. Additional studies will be needed to define the contribution of p38δ to macrophage, neutrophil, and T cell functions, and of p38β to signaling in endothelial cells and T cells.
APA, Harvard, Vancouver, ISO, and other styles
2

Risco, Ana, and Ana Cuenda. "New Insights into the p38γ and p38δ MAPK Pathways." Journal of Signal Transduction 2012 (November 30, 2012): 1–8. http://dx.doi.org/10.1155/2012/520289.

Full text
Abstract:
The mammalian p38 mitogen-activated protein kinases (MAPKs) family is composed of four members (p38α, p38β, p38γ, and p38δ), which are very similar in amino acid sequence but differ in their expression patterns. This suggests that they may have specific functions in different organs. In the last years most of the effort has been centred on the study of the function of the p38α isoform, which is widely referred to as p38 in the literature. However, the role that other p38 isoforms play in cellular functions and their implication in some of the pathological conditions have not been precisely defined so far. In this paper we highlight recent advances made in defining the functions of the two less studied alternative p38MAPKs, p38γ and p38δ. We describe that these p38MAPKs show similarities to the classical p38α isoform, although they may play central and distinct role in certain physiological and pathological processes.
APA, Harvard, Vancouver, ISO, and other styles
3

Adachi-Yamada, Takashi, Makoto Nakamura, Kenji Irie, Yoshinori Tomoyasu, Yorikata Sano, Eiji Mori, Satoshi Goto, Naoto Ueno, Yasuyoshi Nishida, and Kunihiro Matsumoto. "p38 Mitogen-Activated Protein Kinase Can Be Involved in Transforming Growth Factor β Superfamily Signal Transduction in Drosophila Wing Morphogenesis." Molecular and Cellular Biology 19, no. 3 (March 1, 1999): 2322–29. http://dx.doi.org/10.1128/mcb.19.3.2322.

Full text
Abstract:
ABSTRACT p38 mitogen-activated protein kinase (p38) has been extensively studied as a stress-responsive kinase, but its role in development remains unknown. The fruit fly, Drosophila melanogaster, has two p38 genes, D-p38a and D-p38b. To elucidate the developmental function of the Drosophilap38’s, we used various genetic and pharmacological manipulations to interfere with their functions: expression of a dominant-negative form of D-p38b, expression of antisense D-p38b RNA, reduction of theD-p38 gene dosage, and treatment with the p38 inhibitor SB203580. Expression of a dominant-negative D-p38b in the wing imaginal disc caused a decapentaplegic (dpp)-like phenotype and enhanced the phenotype of a dpp mutant. Dpp is a secretory ligand belonging to the transforming growth factor β superfamily which triggers various morphogenetic processes through interaction with the receptor Thick veins (Tkv). Inhibition of D-p38b function also caused the suppression of the wing phenotype induced by constitutively active Tkv (TkvCA). Mosaic analysis revealed that D-p38b regulates the Tkv-dependent transcription of theoptomotor-blind (omb) gene in non-Dpp-producing cells, indicating that the site of D-p38b action is downstream of Tkv. Furthermore, forced expression of TkvCA induced an increase in the phosphorylated active form(s) of D-p38(s). These results demonstrate that p38, in addition to its role as a transducer of emergency stress signaling, may function to modulate Dpp signaling.
APA, Harvard, Vancouver, ISO, and other styles
4

Xing, Feiyue, Yong Jiang, Jing Liu, Kesen Zhao, Yongyan Mo, Zhifeng Liu, and Yaoying Zeng. "Downregulation of human endothelial nitric oxide synthase promoter activity by p38 mitogen-activated protein kinase activation." Biochemistry and Cell Biology 84, no. 5 (October 2006): 780–89. http://dx.doi.org/10.1139/o06-092.

Full text
Abstract:
Human endothelial nitric oxide synthase (eNOS) plays a crucial role in maintaining blood pressure homeostasis and vascular integrity. eNOS gene expression may be upregulated by a signaling pathway, including PI-3Kγ → Jak2 → MEK1 → ERK1/2 → PP2A. It remains unclear whether other mitogen-activated protein kinase (MAPK) family members, such as JNK, p38 kinase, and ERK5/BMK1, also modulate eNOS gene expression. Our purpose, therefore, is to shed light on the effect of the p38 MAPK signaling pathway on the regulation of eNOS promoter activity. The results showed that a red fluorescent protein reporter gene vector containing the full length of the human eNOS promoter was first successfully constructed, expressing efficiently in ECV304 cells with the characteristics of real time observation. The wild-types of p38α, p38β, p38γ, and p38δ signal molecules all markedly downregulated promoter activity, which could be reversed by their negative mutants, including p38α (AF), p38β (AF), p38γ (AF), and p38δ (AF). Promoter activity was also significantly downregulated by MKK6b (E), an active mutant of an upstream kinase of p38 MAPK. The reduction in promoter activity by p38 MAPK could be blocked by treatment with a p38 MAPK specific inhibitor, SB203580. Moreover, the activation of endogenous p38 MAPK induced by lipopolysaccharide resulted in a prominent reduction in promoter activity. These findings strongly suggest that the activation of the p38 MAPK signaling pathway may be implicated in the downregulation of human eNOS promoter activity.
APA, Harvard, Vancouver, ISO, and other styles
5

Roche, Olga, Diego M. Fernández-Aroca, Elena Arconada-Luque, Natalia García-Flores, Liliana F. Mellor, María José Ruiz-Hidalgo, and Ricardo Sánchez-Prieto. "p38β and Cancer: The Beginning of the Road." International Journal of Molecular Sciences 21, no. 20 (October 12, 2020): 7524. http://dx.doi.org/10.3390/ijms21207524.

Full text
Abstract:
The p38 mitogen-activated protein kinase (MAPK) signaling pathway is implicated in cancer biology and has been widely studied over the past two decades as a potential therapeutic target. Most of the biological and pathological implications of p38MAPK signaling are often associated with p38α (MAPK14). Recently, several members of the p38 family, including p38γ and p38δ, have been shown to play a crucial role in several pathologies including cancer. However, the specific role of p38β (MAPK11) in cancer is still elusive, and further investigation is needed. Here, we summarize what is currently known about the role of p38β in different types of tumors and its putative implication in cancer therapy. All evidence suggests that p38β might be a key player in cancer development, and could be an important therapeutic target in several pathologies, including cancer.
APA, Harvard, Vancouver, ISO, and other styles
6

Gonzalez, Maria E., Shilpa R. Tekula, Talha Anwar, Shoshana A. Leflein, and Celina G. Kleer. "Abstract PD3-03: EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression." Cancer Research 82, no. 4_Supplement (February 15, 2022): PD3–03—PD3–03. http://dx.doi.org/10.1158/1538-7445.sabcs21-pd3-03.

Full text
Abstract:
Abstract Introduction: Triple negative breast cancers (TNBC) are frequently poorly differentiated with higher propensity for metastasis than all other subtypes. Enhancer of Zeste Homolog 2 (EZH2) is a lysine methyltransferase that mediates transcriptional repression of pro-differentiation genes in normal and neoplastic cells. The oncogenic role of EZH2 through H3K27me3 is well established. However, non-canonical H3K27me3-independent functions are unclear. We have reported that p38 phosphorylates T367 of EZH2, increasing TNBC metastasis. Recent reports show that EZH2 can regulate signaling pathways through direct methylation of proteins suggesting the hypothesis that EZH2 may methylate p38 in TNBC. Methods: Human tissue samples from 16 primary invasive breast carcinomas and matched distant metastasis arrayed in tissue microarrays were interrogated for pEZH2 T367 and p-p38 by immunohistochemistry. To study p38 methylation, we performed LC-MS/MS analyses GST-p38α, and GST-EZH2 were each incubated with or without recombinant PRC2 complex (EZH2/E ED/SUZ12/RbAp48/AEBP2) and S-adenosyl methionine methyl donor. MDA-MB-231, mouse and human primary TNBC cells and murine 4T1 cells were used in funcional assays in vitro and in vivo. EZH2 knockdown and rescue was carried out using lentiviral transduction of EZH2 with pBabe-myc-EZH2 (wild-type) or pBabe-myc-EZH2 (T367A). We developed p38 methylation mutants: HA-p38a K139A, HA-p38a K165A, and HA-p38a K130A/K165K. To investigate the importance of EZH2 and p38 enzymatic activities we used the EZH2 methyltransferase inhibitors GSK-343 and EPZ-6438 and the p38 inhibitor SB202190 in vitro and in vivo. For animal studies, MDA-MB-231 and 4T1 cells were orthotopically injected into the right inguinal mammary fat pad of eight-week old NOD/SCID or BALBc mice, respectively. When tumors reached 100 mm3 mice were treated 5 days/week by intraperitoneal injection with SB202190 (1mg/kg/day), EPZ-6438 (10mg/kg/day), combination of SB202190 and EPZ-6438, or control. We monitored tumor growth for 50 days, and harvested primary tumors, lungs, and sites of metastasis for histopathology, Western blot, and immunohistochemistry. Primary xenografts from the control and treatment groups were subjected to RNA sequencing. Results: EZH2 methylates p38 at lysines 139 and 165 leading to enhanced p38 stability and increased invasion, and p38 activation requires T367 phosphorylation of EZH2. Dual inhibition of EZH2 methyltransferase and p38 kinase activities downregulates pEZH2 T367, H3K27me3, and p-p38 in vivo, reduces TNBC growth and metastasis, and results in gene expression changes towards a better differentiated phenotype. pEZH2 T367 and p-p38 proteins are significantly coexpressed in human primary and metastatic breast cancer. Conclusions: We provide direct evidence that EZH2 methylates p38 with resultant p38 activation, and that EZH2 phosphorylation at T367 is important for this function. Dual targeting of EZH2 methyltransferase and p38 kinase activities with specific inhibitors reduces breast cancer growth and metastasis indicating a cooperation between EZH2 canonical and non-canonical mechanisms and suggesting therapeutic strategies. Citation Format: Maria E Gonzalez, Shilpa R. Tekula, Talha Anwar, Shoshana A. Leflein, Celina G. Kleer. EZH2 T367 phosphorylation activates p38 signaling through lysine methylation to promote breast cancer progression [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr PD3-03.
APA, Harvard, Vancouver, ISO, and other styles
7

Gutierrez-Sanmartin, Dolores, Eduardo Varela-Ledo, Antonio Aguilera, Susana Romero-Yuste, Patricia Romero-Jung, Antonio Gomez-Tato, and Benito J. Regueiro. "Implication of p38 mitogen-activated protein kinase isoforms (α, β, γ and δ) in CD4+ T-cell infection with human immunodeficiency virus type I." Journal of General Virology 89, no. 7 (July 1, 2008): 1661–71. http://dx.doi.org/10.1099/vir.0.82971-0.

Full text
Abstract:
The CD4+ T-cell reduction characteristic of human immunodeficiency virus type 1 (HIV-1) infection is thought to result, in addition to infected T-cell death, mainly from uninfected bystander T-cell apoptosis. Nevertheless, the immunological and virological mechanisms leading to T-cell death during HIV-1 infection are not yet fully understood. In the present study, we analysed the individual implication of the p38 mitogen-activated protein kinase (MAPK) isoforms (p38α, p38β, p38γ and p38δ) during apoptosis induced by HIV-1, taking into account that HIV-1 replication is known to be blocked by p38 inhibitors. For this purpose, we used the SupT1 cell line, where death induced by HIV-1 mainly occurs by uninfected bystander cell apoptosis. A variety of SupT1-based cell lines were constructed constitutively expressing, under the control of cytomegalovirus promoter (PCMV), each dominant-negative (dn) p38 isoform and each wild-type p38 isoform as a control. An enhanced green fluorescent protein marker gene, under the control of the HIV-1 promoter, was inserted in all of them. These cell lines were infected with HIV-1 and analysed by flow cytometry. We found that survival in SupT1-based cell lines infected by HIV-1 was increased by the p38αdn, p38γdn and p38δdn isoforms, but not by the p38βdn isoform. HIV-1 replication was delayed most by p38δdn and to a lesser extent by p38αdn and p38γdn. Moreover, these three isoforms, p38αdn, p38γdn and p38δdn, reduced apoptosis induced by HIV-1. These results suggest that, in SupT1-based cell lines, p38α, p38γ and p38δ, but not p38β, are implicated in both HIV-1 induced replication and apoptosis in infected and uninfected bystander cells.
APA, Harvard, Vancouver, ISO, and other styles
8

KUMA, Yvonne, David G. CAMPBELL, and Ana CUENDA. "Identification of glycogen synthase as a new substrate for stress-activated protein kinase 2b/p38beta." Biochemical Journal 379, no. 1 (April 1, 2004): 133–39. http://dx.doi.org/10.1042/bj20031559.

Full text
Abstract:
The endogenous glycogen synthase in extracts from mouse skeletal muscle, liver and brain bound specifically to SAPK2b (stress-activated protein kinase 2b)/p38β, but not to other members of the group of SAPK/p38 kinases. Glycogen synthase was phosphorylated in vitro more efficiently by SAPK2b/p38β than by SAPK2a/p38α, SAPK3/p38γ or SAPK4/p38δ. SAPK2b/p38β phosphorylated glycogen synthase in vitro at residues Ser644, Ser652, Thr718 and Ser724, two of which (Ser644 and Ser652) are also phosphorylated by glycogen synthase kinase 3. Thr718 and Ser724 are novel sites not known to be phosphorylated by other protein kinases. Glycogen synthase becomes phosphorylated at Ser644 in response to osmotic shock; this phosphorylation is prevented by pretreatment of the cells with SB 203580, which inhibits SAPK2a/p38α and SAPK2b/p38β activity. In vitro, phosphorylation of glycogen synthase by SAPK2b/p38β alone had no significant effect on its activity, indicating that phosphorylation at residue Ser644 itself is insufficient to decrease glycogen synthase activity. However, after phosphorylation by SAPK2b/p38β, subsequent phosphorylation at Ser640 by glycogen synthase kinase 3 decreased the activity of glycogen synthase. This decrease was not observed when SAPK2b/p38β activity was blocked with SB 203580. These results suggest that SAPK2b/p38β may be a priming kinase that allows glycogen synthase kinase 3 to phosphorylate Ser640 and thereby inhibit glycogen synthase activity.
APA, Harvard, Vancouver, ISO, and other styles
9

Thouverey, Cyril, and Joseph Caverzasio. "Ablation of p38α MAPK Signaling in Osteoblast Lineage Cells Protects Mice From Bone Loss Induced by Estrogen Deficiency." Endocrinology 156, no. 12 (October 6, 2015): 4377–87. http://dx.doi.org/10.1210/en.2015-1669.

Full text
Abstract:
Estrogen deficiency causes bone loss by increasing the number of bone-resorbing osteoclasts. Selective p38α MAPK inhibitors prevent bone-wasting effects of estrogen withdrawal but implicated mechanisms remain to be identified. Here, we show that inactivation of the p38α-encoding gene in osteoblast lineage cells with the use of an osteocalcin-cre transgene protects mice from ovariectomy-induced bone loss (a murine model of postmenopausal osteoporosis). Ovariectomy fails to induce bone loss, increase bone resorption, and stimulate receptor activator of nuclear factor κB ligand and IL-6 expression in mice lacking p38α in osteoblasts and osteocytes. Finally, TNFα or IL-1, which are osteoclastogenic cytokines overproduced in the bone marrow under estrogen deficiency, can activate p38α signaling in osteoblasts, but those cytokines cannot enhance Rankl and Il6 expressions or increase osteoclast formation in p38a-deficient osteoblast cultures. These findings demonstrate that p38α MAPK signaling in osteoblast lineage cells mediates ovariectomy-induced bone loss by up-regulating receptor activator of nuclear factor κB ligand and IL-6 production.
APA, Harvard, Vancouver, ISO, and other styles
10

Lovett, Fiona A., Ruth A. Cosgrove, Ivelisse Gonzalez, and Jennifer M. Pell. "Essential Role for p38α MAPK But Not p38γ MAPK in Igf2 Expression and Myoblast Differentiation." Endocrinology 151, no. 9 (July 7, 2010): 4368–80. http://dx.doi.org/10.1210/en.2010-0209.

Full text
Abstract:
The muscle satellite cell is established as the major stem cell contributing to fiber growth and repair. p38 MAPK signaling is essential for myoblast differentiation and in particular for up-regulation of promyogenic Igf2 expression. p38 exists as four isoforms (α, β, γ, and δ), of which p38γ is uniquely abundant in muscle. The aim of this study was to characterize p38 isoform expression and importance (using shRNA knockdown; demonstrated via both reduced protein and kinase activities) during myoblast differentiation. p38α and -γ mRNA levels were most abundant in differentiating C2 cells with low/negligible contributions from p38β and -δ, respectively. Increased phosphorylation of p38α and -γ occurred during differentiation but via different mechanisms: p38α protein levels remained constant, whereas total p38γ levels increased. Following shRNA knockdown of p38α, myoblast differentiation was dramatically inhibited [reduced myosin heavy chain (MHC), myogenin, pAkt protein levels]; significantly, Igf2 mRNA levels and promoter-reporter activities decreased. In contrast, knockdown of p38γ induced a transient increase in both myogenin and MHC protein levels with no effect on Igf2 mRNA levels or promoter-reporter activity. Knockdown of p38α/β markedly increased but that of p38γ decreased caspase 3 activity, suggesting opposite actions on apoptosis. p38γ was initially proposed to have a promyogenic function; however, p38γ overexpression could not rescue reduced myoblast differentiation following p38α/β inhibition. Therefore, p38α is essential for myoblast differentiation, and part of its action is to convert signals that indicate cell density into promyogenic gene expression in the form of the key peptide, IGF-II; p38γ has a minor, yet opposing antimyogenic, function.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "P38a"

1

Gutierrez, Prat Núria. "Molecular basis of p38a MAPK signaling." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/663438.

Full text
Abstract:
Cells often need to respond to damaging internal and external stimuli. One of the pathways that is frequently activated by stress stimuli involves activation of the kinase p38alpha, which can phosphorylate different substrates, including MK2. Experiments using purified proteins have shown that non-phosphorylated p38alpha and MK2 can form a tight complex, in which structural constraints impede the interaction of both kinases with effectors and regulators. It is therefore critical to understand how the interaction between p38alpha and MK2 is regulated to ensure that they can release from each other and phosphorylate the required substrates that mediate their functions. Here, we show that in cells under homeostatic conditions, endogenous p38alpha and MK2 form a stable complex that is disrupted upon phosphorylation of both proteins. The separation of the two kinases causes MK2 destabilization and degradation by the proteasome in a MDM2-dependent manner. Depending on the intensity of the stimuli, p38alpha and MK2 undergo different fates. Transient stimulation leads to complex separation and MK2 degradation followed by increased MK2 expression, and the eventual reassembly of the p38alpha:MK2 complex. On the contrary, in cells exposed to strong stimuli that lead to sustained p38alpha activation, as it is often the case with stress, both kinases remain phosphorylated, cannot bind to each other and eventually become destabilized, being unable to recover the steady state. Taken together, our results illustrate a new mechanism of p38alpha signaling regulation based on the p38alpha:MK2 complex dynamics, which may have implications for different processes regulated by p38alpha and MK2 signaling.
APA, Harvard, Vancouver, ISO, and other styles
2

Renaud, Emilie. "Inhibition isoforme spécifique des fonctions de la MAPK p38α par des fragments d’anticorps." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT088.

Full text
Abstract:
La MAPK p38α est une protéine clé de l’inflammation, également impliquée dans de nombreux processus liés au cancer. Les petites molécules chimiques inhibitrices de p38α bloquent son activité kinase par un mécanisme de compétition à l’ATP. En raison de la grande conservation du domaine kinase, la spécificité de la majorité de ces inhibiteurs n’est pas restreinte à la p38α et des effets « off-targets » ont été rapportés. Dans ce contexte, le projet de ma thèse a porté sur l’utilisation de fragments d’anticorps au format scFv comme nouvel outil de ciblage pharmacologique afin de définir une/des voie(s) alternative(s) d’inhibition de la p38α. Les fragments d’anticorps lient un motif antigénique avec une affinité et une spécificité élevées, tout comme les immunoglobulines classiques. Leur expression intracellulaire permet également le ciblage de protéines cytoplasmiques et l’étude de leurs fonctions dans des processus physiologiques et pathologiques. Nous avons sélectionné par phage display, à partir d’une banque de fragments d’anticorps, 5 scFv spécifiques de la MAPK p38α. Alors que tous ces scFv empêchent l’activation par phosphorylation de la p38α par MKK6, l’un d’entre eux agit directement sur l’enzyme pour inhiber totalement son activité kinase in vitro. Ce scFv possède un site de liaison et un mécanisme d’inhibition distincts des inhibiteurs pharmacologiques déjà décrits : bien qu’il ne cible pas le domaine kinase et n’empêche pas la fixation de l’ATP, le scFv se comporte comme un inhibiteur compétitif de l’hydrolyse de l’ATP. Ces résultats suggèrent un effet allostérique du scFv sur l’activité de la p38α et permettent de le caractériser comme un inhibiteur compétitif non conventionnel. La détermination de son épitope d‘interaction ainsi que la confirmation de sa fonctionnalité une fois exprimé dans le cytosol des cellules nous permettra de définir une voie alternative d'inhibition de la p38α et de valider notre approche de ciblage par l’utilisation de fragments d’anticorps.Ces données ouvrent de nouvelles perspectives de design d’inhibiteurs chimiques de la p38α de meilleure spécificité que ceux actuellement disponibles
MAPK p38α is a key protein in inflammation, but is also involved in many cancer-related processes. All the currently described chemical inhibitors of p38α inhibit its kinase activity by an ATP-competitive mechanism. Because of the high conservation of the ATP-binding pocket, the majority of these inhibitors are not specific to p38α and off-target effects have been reported. To identify alternative approaches to inhibit p38α MAPK, my thesis project focused on the use of scFv antibody fragments as a new highly specific pharmacological tool.Antibody fragments bind to an antigen with high affinity and specificity like conventional immunoglobulins. Their intracellular expression also allows to target cytoplasmic proteins and study the target functions in physiological and pathological processes. Using a naïve library of antibody fragments, we have selected by phage display five scFv specific of MAPK p38α isoform. While all these scFv inhibit the activation of p38α by MMK6, one of them also completely inhibits its kinase activity in vitro. This scFv has a binding site and a mechanism of inhibition distinct from the pharmacological inhibitors currently described: although it does not target the ATP-binding pocket and does not prevent ATP binding, it behaves like a competitive inhibitor of ATP hydrolysis. These results suggest an allosteric effect of this scFv on p38α activity and allow to characterize it as an unconventional competitive inhibitor. The determination of its epitope as well as the confirmation of its inhibitory activity once expressed in the cell cytosol will allow us to propose an alternative approach to target p38α function using antibody fragments.These data open up new perspectives for the design of more specific p38α chemical inhibitors than those currently available
APA, Harvard, Vancouver, ISO, and other styles
3

Visseq, Alexia. "Conception et synthèse d’inhibiteurs sélectifs de protéines kinases pour le traitement de l’allodynie mécanique." Thesis, Université Clermont Auvergne‎ (2017-2020), 2019. http://www.theses.fr/2019CLFAC048.

Full text
Abstract:
La douleur chronique constitue aujourd’hui un problème majeur de santé publique qui touche près de 20% de la population. L’allodynie mécanique, une douleur provoquée par une stimulation normalement non douloureuse, est le symptôme le plus fréquent chez les patients atteints de douleur chronique. Malheureusement, les traitements actuellement disponibles ne sont pas réellement efficaces ou bien présentent d’importants effets secondaires ou contre-indications. L’objectif de ce projet est de concevoir, synthétiser et évaluer biologiquement des inhibiteurs sélectifs de protéines kinases pour le traitement de l’allodynie mécanique. Au cours de ce travail de thèse, nous avons découvert de nouveaux inhibiteurs sélectifs de p38α, une protéine kinase bien connue pour son implication dans la douleur chronique et l’allodynie mécanique. Une étude des relations structure-activités a été réalisée pour identifier les éléments structuraux importants permettant d’améliorer l’activité des molécules in vitro et in vivo sur un modèle animal. Les meilleures molécules ont présenté des IC50 submicromolaires sur p38α et une forte inhibition de l’allodynie mécanique in vivo
Chronic pain is a global public health priority which affects more than 20% of Europeans. Mechanical allodynia, a pain in response to normally innocuous stimuli, is one of the most prevalent pain symptoms. Despite intensive research toward the study of pain mechanisms, currently available treatments of pain are not always effective, and can produce side-effects. In this context, the aim of the project is to design, synthesize and evaluate selective inhibitors of protein kinases for the treatment of mechanical allodynia. During this PhD work, new selective inhibitors of the protein kinase p38α has been discovered. This protein kinase is known for its implication in chronic pain and mechanical allodynia. A structure-activity relationship study was performed to identify the important structural features allowing a gain of activity of molecules in vitro and in vivo using an animal model. The best compounds showed submicromolar IC50 values toward p38α and a strong inhibition of mechanical allodynia in vivo
APA, Harvard, Vancouver, ISO, and other styles
4

Vitos, Faleato Jessica. "Role of p38α in lung tumor progression." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/462107.

Full text
Abstract:
Tumors evolve by sequentially acquiring genetic abnormalities, like K-Ras activation and Tp53 loss of function, which enable transformed cells to survive, proliferate, invade, and reprogram their microenvironment. Simultaneously, transformed cells need to cope with a stressful scenario, including an accelerated metabolism, genome instability, or immune surveillance. Therefore, cancer cells must rely on some non-oncogenic signaling pathways to tolerate homeostatic control deficiencies, adapt to the new demands, and monitor continuous changes in the microenvironment to respond accordingly. The p38 MAPK signaling pathway is a stress-related pathway that cells use to transduce extracellular cues and orchestrate appropriate responses. p38α, the most widely expressed p38 MAPK family member, has been classically attributed tumor suppressor functions due to its ability to arrest the cell cycle, induce cell differentiation, and trigger apoptosis. Nevertheless, in several human tumor types, p38 MAPK activity levels have been found increased and sometimes correlated to poor survival, suggesting a pro-tumorigenic role. In this study, we observed a negative correlation between p38α mRNA expression levels and the overall survival of lung adenocarcinoma patients. Using a K-RasG12V driven mouse model of lung cancer, we show that indeed p38α signaling plays a dual role during lung tumorigenesis. On one hand, p38α avoids malignant transformation in lung epithelial cells by promoting their differentiation. However, in the transformed lung epithelial cells, p38α enhances proliferation as well as the secretion of inflammatory cytokines to form a favorable niche for cancer progression. p38α also plays a pro-tumorigenic role by promoting tumor vascularization and immunotolerance of tumor-infiltrated myeloid cells. Altogether, our data suggest that targeting this pathway might be therapeutically useful for lung adenocarcinoma.
Los tumores evolucionan al adquirir anormalidades genéticas de manera secuencial, como la activación de K-Ras y la pérdida de funcionalidad de Tp53, que permiten a las células transformadas sobrevivir, proliferar, e invadir, así como acondicionar su microambiente. Simultáneamente, las células transformadas también han de lidiar con situaciones de estrés, incluyendo un metabolismo acelerado, un genoma altamente inestable, o el sistema de vigilancia de las células inmunes. Por lo tanto, las células cancerosas han de apoyarse en vías de señalización no-oncogénicas que les permiten tolerar las deficiencias en los sistemas de control de homeostasis, adaptarse a los nuevos requerimientos funcionales, y monitorizar los cambios en el microambiente para responder de manera apropiada. La vía de las p38 MAPK está íntimamente relacionada con la respuesta al estrés y es utilizada por las células para transducir señales extracelulares y orquestrar las respuestas correspondientes. p38α es el miembro de la familia de p38 MAPK más ampliamente expresado, y se le han atribuido clásicamente funciones supresoras tumorales gracias a su habilidad para detener el ciclo celular, inducir diferenciación, y desencadenar procesos apoptóticos. No obstante, hay evidencia de que el nivel de actividad de p38 MAPK podría estar incrementado en varios tipos de tumor humanos y, en algunos casos, se ha correlacionado con una baja supervivencia, lo que sugiere un papel pro-tumoral. En este estudio, hemos observado una correlación negativa entre los niveles de expresión de p38α y la supervivencia en pacientes de adenocarcinoma pulmonar. Hemos usado un modelo murino de cáncer de pulmón inducido por la expresión del oncogén K-Ras para demostrar que, efectivamente, p38α juega un papel dual durante el desarrollo de la carcinogénesis de pulmón. Por una parte, p38α evita la transformación maligna de las células pulmonares epiteliales sanas mediante la inducción de diferenciación celular. Sin embargo, en las células epiteliales pulmonares transformadas, p38α estimula la proliferación y la secreción de citocinas inflamatorias que preparan un nicho favorable para la progresión tumoral. p38α también juega un rol pro-tumorigénico al promover la vascularización del tumor y la immunotolerancia por parte de las células mieloides infiltradas. En conjunto, nuestros datos sugieren que la inhibición de esta vía de señalización podría ser útil en términos terapéuticos para los casos de adenocarcinoma de pulmón.
APA, Harvard, Vancouver, ISO, and other styles
5

Thapa, Dibesh. "Targeting the interaction between p38α and TAB1." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/targeting-the-interaction-between-p38-and-tab1(9b1a1609-805a-4698-a673-2a686dabf905).html.

Full text
Abstract:
p38α, a member of the mitogen activated protein kinase family, is a stress activated serine/threonine kinase which plays an important role in signalling pathways mediating fundamental processes such as inflammation, apoptosis, autophagy, and cell division, differentiation and death. Over the last two decades, its prominence in ischaemic heart disease has risen rapidly with several studies providing overwhelming evidence that p38α activation aggravates lethal injury during myocardial ischaemia. Several inhibitors have been tested to prevent p38α activation and although they have performed well in the laboratory; unfortunately the results have not translated to clinical trials in patients. This has mainly been due to toxicity such as liver injury, skin rashes, gastrointestinal disorders, and flares-ups of rheumatoid arthritis. These adverse effects are shared by different inhibitors, the majority of which belong to the ATP-mimetic, type I group, suggesting they result from an on-target effect of inhibiting ubiquitously expressed p38α. As a result, an alternative therapeutic strategy, other than the blanket inhibition of p38, is required. TAB1 mediated p38α activation appears to be the culprit behind the detrimental p38α signalling during myocardial ischaemia and selectively targeting this branch of p38α activation, without affecting prototypical p38α activation, is highly desirable. In this thesis I studied the structural features of p38α and TAB1 which contribute to the TAB1-mediated p38α autoactivation mechanism. Using various biochemical and biophysical tools in in-vitro and ex-vivo systems, I have identified the key residue in p38α, and TAB1, which contribute to the auto-activation of p38α by TAB1. The results from my investigations suggest that targeting these residues impairs the autoactivation process and these structural features may be exploited to elucidate p38α’s role in myocardial ischaemia. Ischaemic heart disease continues to be the biggest killer in the world, and the search for p38α inhibitors still continues without any fruitful outcomes. A new direction and strategy focusing on circumstance selective inhibition is required in p38α therapeutics, and hopefully the results in my thesis will contribute to that search.
APA, Harvard, Vancouver, ISO, and other styles
6

Mäkelä, Kimmo K. "Characterization and performance of electrorheological fluids based on pine oils /." Espoo, Finland : University of Oulu, 1999. http://www.vtt.fi/inf/pdf/publications/1999/P385.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Heikkilä, Anna-Mari. "Inherent safety in process plant design : an index-based approach /." Espoo [Finland] : Technical Research Centre of Finland, 1999. http://www.vtt.fi/inf/pdf/publications/1999/P384.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Uosukainen, Seppo. "JMC method applied to active control of sound : theoretical extensions and new source configurations /." Espoo [Finland] : Technical Research Centre of Finland, 1999. http://www.vtt.fi/inf/pdf/publications/1999/P386.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Patil, Ashok R. "High power shunt regulation of spacecraft solar arrays." Diss., Virginia Tech, 1995. http://hdl.handle.net/10919/40216.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Patterson, Douglas T. "Tribopolymerization as an approach to two-stroke engine lubrication." Thesis, This resource online, 1995. http://scholar.lib.vt.edu/theses/available/etd-01312009-063142/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "P38a"

1

Ross, Herbert E. Adventures of a P38 ace. Stockton, CA: Graphics West Printing, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

1946-, Cerocchi Pio, ed. La P38 e la mela: Una presenza cristiana a Roma negli anni di piombo. Castel Bolognese (RA) [i.e. Ravenna, Italy]: Itaca, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Purnama, Eddy. Pembentukan dan pembinaan P3A beririgasi di Kabupaten Daerah Tingkat II Aceh Utara: Laporan penelitian. [Banda Aceh]: Fakultas Hukum, Universitas Syiah Kuala, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Muliawati, Endang Setia. Studi pengembangan perkumpulan petani pemakai air (P3A) dalam pengelolaan sumberdaya air dan lahan: Laporan penelitian. Surakarta: Fakultas Pertanian, Universitas Sebelas Maret, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hermajanda, Dadan. Keragaan organisasi Perkumpulan Petani Pemakai Air (P3A) sepanjang Sungai Cisangkuy, Kabupaten Bandung, Jawa Barat: Laporan penelitian. Bandung: Pusat Dinamika Pembangunan, Universitas Padjadjaran, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Furtak, Teresa. Role of p38 MAP kinase in apoptosis in L-glutamine deprived SP2/0-Ag14 mouse hybridoma cells. Sudbury, Ont: Laurentian University, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Andriani, Haslinda B. Motivasi masyarakat dalam pembentukan perkumpulan petani pemakai air (P3A) di Kecamatan Parigi, Kabupaten Parigi Moutong: Laporan penelitian dosen muda. [Palu]: Fakultas Ilmu Sosial dan Ilmu Politik, Universitas Tadulako, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Naldi, Hendra. Pengaruh pelatihan perkumpulan petani pemakai air (P3A) terhadap partisipasi wanita tani dalam kegiatan pengelolaan irigasi di daerah irigasi Batang Anai, Padang Pariaman: Laporan penelitian. [Padang]: Institut Keguruan dan Ilmu Pendidikan Padang, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Walther P38 Pistol. Naval & Military Press, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

P38 Signaling Pathway. MDPI, 2021. http://dx.doi.org/10.3390/books978-3-0365-0859-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "P38a"

1

Cha, Hyuk-Jin, and Albert J. Fornace. "P38." In Cancer Therapeutic Targets, 805–15. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_85.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Cha, Hyuk-Jin, and Albert J. Fornace. "P38." In Cancer Therapeutic Targets, 1–11. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6613-0_85-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "P-38α (Phospho p38α)." In Encyclopedia of Signaling Molecules, 1331. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100980.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Qi, Xiao-Mei, Fang Wang, and Guan Chen. "p38 Gamma MAPK." In Encyclopedia of Signaling Molecules, 3718–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101521.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Papaconstantinou, John, Ching-Chyuan Hsieh, and James H. DeFord. "p38 MAPK Family." In Encyclopedia of Signaling Molecules, 3728–39. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_221.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Qi, Xiao-Mei, Fang Wang, and Guan Chen. "p38 Gamma MAPK." In Encyclopedia of Signaling Molecules, 1–11. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101521-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Papaconstantinou, John, Ching-Chyuan Hsieh, and James H. DeFord. "p38 MAPK Family." In Encyclopedia of Signaling Molecules, 1–12. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_221-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Waud, William R. "Murine L1210 and P388 Leukemias." In Tumor Models in Cancer Research, 23–41. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Waud, William R. "Murine L1210 and P388 Leukemias." In Anticancer Drug Development Guide, 79–97. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-739-0_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Waud, William R. "Murine L1210 and P388 Leukemias." In Anticancer Drug Development Guide, 59–74. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4615-8152-9_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "P38a"

1

Tsai, Ying-Kuan, and Richard J. Malak. "A Constraint-Handling Technique for Parametric Optimization and Control Co-Design." In ASME 2022 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/detc2022-89957.

Full text
Abstract:
Abstract This paper proposes a novel technique for handling constraints in population-based algorithms (e.g., genetic algorithms) for parametric optimization and control co-design (CCD). Constraint boundaries are approximated during optimization using a machine-learning classification approach called a support vector machine (SVM). Population members classified as infeasible are shifted to the predicted boundary of the feasible set, promoting exploration in the most important regions of the search space. A numerical test problem and a case study of an elastic inverted pendulum on a cart are used for benchmarking. The inverted pendulum problem, which features inherently unstable dynamics and control system limitations (i.e., saturation), highlights the relevance of constraint handling in CCD problems. The case study includes constraints to ensure stability and account for controller saturation. Performance and computational cost are compared to the existing parametric optimization technique, Predicted Parameterized Pareto Genetic Algorithm (P3GA). Results show that the P3GA with the newly proposed constraint-handling technique outperforms the original P3GA both qualitatively and quantitatively.
APA, Harvard, Vancouver, ISO, and other styles
2

Reynolds, Claire, Molly Cremin, and Susanna Felsenstein. "P382 Thinking outside the POX." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.728.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Figueirinha, Joana, Sara Rolim, Ana Sofia Gomes, Filipa Pinto, and Paulo Teixeira. "P384 More than meets the eye." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.730.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Barbee, Kenneth A., Gulyeter Serbest, and Joel Horwitz. "Membrane Integrity as a Therapeutic Target in Neural Cell Injury." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61566.

Full text
Abstract:
The importance of cell membrane integrity for normal cell function and indeed survival is well established, yet the role of membrane disruption in cellular pathology is seldom considered except as a prelude to, or indication of, cell death. However, evidence from diverse fields strongly implicates membrane disruption as a key precipitating event in the pathological responses to various stimuli. Dynamic mechanical loading of neural cells produces an acute disruption of the plasma membrane as indicated by a rapid and transient release of LDH from the cytoplasm of injured cells. In this report, we show that this cellular level injury is not immediately fatal, but rather gives rise to a cascade of signaling events that lead to cell death in the long term. In our model, over 50% of the cells were dead at 24 hours post injury, the majority of which were apoptotic as assessed by the TUNEL assay using flow cytometry. Though many of the signaling pathways involved in this response to injury have been studied, the link between the initial membrane damage and the subsequent signaling is poorly understood. We report for the first time that treating injured neurons with an agent that promotes resealing of membrane pores can rescue the cells from both necrotic cell death and apoptosis at 24 hours post injury. Treatment with the nonionic surfactant, poloxamer 188 (P188), at 15 minutes post injury restored cell viability at 24 hours to control values. The role of the pro-apoptosis MAP kinase, p38, in cell death following injury was investigated using Western blot analysis. Activation of p38 was increased over 2-fold at 15 minutes post injury. P188 treatment at 10 minutes inhibited p38 activation. However, treatment with a specific inhibitor of p38 activation produced only a partial reduction in apoptosis and had no effect on necrotic cell death. These data suggest multiple signaling pathways are involved in the long term response of neurons to mechanical injury. Furthermore, the putative mechanism of action of P188 to promote membrane resealing suggests that the acute membrane damage due to trauma is a critical precipitating event lying upstream of the many signaling cascades that contribute to the subsequent pathology.
APA, Harvard, Vancouver, ISO, and other styles
5

Zeh, G., M. Köhne, T. Sauerwald, H. Haug, and B. Lok. "P38 - Entwicklung instrumenteller Geruchsmessung." In 16. Dresdner Sensor-Symposium 2022. AMA Service GmbH, Von-Münchhausen-Str. 49, 31515 Wunstorf, Germany, 2022. http://dx.doi.org/10.5162/16dss2022/p38.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Gaspar, P., J. Rowley, A. Pati Pascom, F. Martinez, E. Korenromp, G. Mendes Pereira, and A. Miranda. "P381 Estimating adult gonorrhea prevalence in Brazil." In Abstracts for the STI & HIV World Congress, July 14–17 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/sextrans-2021-sti.416.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

Full text
Abstract:
Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.
APA, Harvard, Vancouver, ISO, and other styles
8

Conlon, Kevin, Molly Cremin, Daragh Finn, Clodagh Ryan, Michael Moore, and Niamh McSweeney. "P383 Stroke in children; consider parvovirus B19 infection." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.729.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Cama, Valeria, Luisa Pieragostini, Giovanna Fontanelli, Maria Rosa Velletri, and Calafiore Mariarosa. "P387 Clostridium difficile severe infection in a newborn." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.733.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

"REVERSE LOGISTICS OF TEŠANJ – WASTE MANAGEMENT SYSTEM." In Transport for Today's Society. Faculty of Technical Sciences Bitola, 2019. http://dx.doi.org/10.20544/tts2018.p38.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "P38a"

1

Bakin, Andrei V. P38 Mitogen-Activated Protein Kinase in Metastasis Associated With Transforming Growth Factor Beta. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada443019.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Bakin, Andrei. p38 Mitogen-Activated Protein Kinase in Metastasis Associated with Transforming Growth Factor Beta. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada456265.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bakin, Andrei V. P38 Mitogen-Activated Protein Kinase in Metastasis Associated with Transforming Growth Factor Beta. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427109.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bakin, Andrei V. P38 Mitogen-Activated Protein Kinase in Metastasis Associated With Transforming Growth Factor Beta. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417915.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Vanhoy, Lyndsay. The SDF1-CXCR4 Axis Functions through p38-MAPK Signaling to Drive Breast Cancer Progression and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada495339.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Vanhoy, Lyndsay. The SDF1-CXCR4 Axis Functions through p38-MAPK Signaling to Drive Breast Cancer Progression and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada517434.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lofgren, Kristopher. Investigation of the Role of Breast Tumor Kinase (Brk) in ERK5 and p38-Mediated Breast Cancer Cell. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada484006.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'P38a' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography