Relevant bibliographies by topics / PIK3R1

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'PIK3R1'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'PIK3R1.'

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 "PIK3R1"

1

Kim, Jin-Mo, Hyun Yoo, Jee-Youn Kim, Sang Ho Oh, Jeong Wook Kang, Byung Rok Yoo, Song Yee Han, et al. "Metformin Alleviates Radiation-Induced Skin Fibrosis via the Downregulation of FOXO3." Cellular Physiology and Biochemistry 48, no. 3 (2018): 959–70. http://dx.doi.org/10.1159/000491964.

Full text
Abstract:
Background/Aims: Radiation-induced skin fibrosis is a common side effect of clinical radiotherapy. Our previous next-generation sequencing (NGS) study demonstrated the reduced expression of the regulatory α subunit of phosphatidylinositol 3-kinase (PIK3r1) in irradiated murine skin. Metformin has been reported to target the PIK3-FOXO3 pathway. In this study, we investigated the effects of metformin on radiation-induced skin fibrosis. Methods: Metformin was orally administered to irradiated mice. Skin fibrosis was analyzed by staining with H&E and Masson’s trichrome stain. The levels of cytokines and chemokines associated with fibrosis were analyzed by immunohistochemistry and quantitative RT-PCR. The roles of PIK3rl and FOXO3 in radiation-induced skin fibrosis were studied by overexpressing PIK3rl and transfecting FOXO3 siRNA in NIH3T3 cells and mouse-derived dermal fibroblasts (MDF). Results: The oral administration of metformin significantly reduced radiation-induced skin thickening and collagen accumulation and significantly reduced the radiation-induced expression of FOXO3 in murine skin. Additionally, the overexpression of PIK3r1 reduced the radiation-induced expression of FOXO3, while FOXO3 silencing decreased the radiation-induced expression of TGFβ in vitro. Conclusions: The results indicated that metformin suppresses radiation-induced skin injuries by modulating the expression of FOXO3 through PIK3r1. Collectively, the data obtained in this study suggested that metformin could be a potent therapeutic agent for alleviating radiation-induced skin fibrosis.
APA, Harvard, Vancouver, ISO, and other styles
2

Dirican, Ebubekir, İpek Erbarut Seven, Handan Kaya, M. Ümit Uğurlu, İrem Peker, Bahadır M. Güllüoğlu, Ayşe Özer, and Mustafa Akkiprik. "PIK3CA and TP53 MUTATIONS and SALL4, PTEN and PIK3R1 GENE EXPRESSION LEVELS in BREAST CANCER." Turkish Journal of Biochemistry 45, no. 5 (March 2, 2020): 515–23. http://dx.doi.org/10.1515/tjb-2019-0137.

Full text
Abstract:
AbstractObjectiveA high frequency of PI3K signalling pathway abnormalities and TP53 mutations are critical in the development and progression of breast cancer (BCa). We aimed to detect PIK3CA and TP53 mutations via an expression analysis of PIK3R1, PTEN and SALL4 and correlate the expression of these genes with clinical parameters of BCa.Materials and methodsPIK3CA and TP53 mutations in BCa samples were analysed by High-Resolution Melting (HRM) analysis, followed by Sanger sequencing, and the expression levels of PIK3R1, PTEN and SALL4 were evaluated by RT-PCR methods.ResultsThe frequency of PIK3CA and TP53 mutations was 42% and 38% according to the HRM and Sanger sequencing. There was a significantly high frequency of these mutations in ER( +), N0 and HER2( −) tumour samples. PIK3R1 and PTEN expression levels were high in tumour samples, whereas SALL4 expression was low. In patients with TP53 mutations, PIK3R1 expression was low, and this finding was statistically significant. PIK3R1 and PTEN expression levels showed statistically significant, respectively in G3 grades, ER(+), (PR)( +), HER2(+) and ER( +).ConclusionsWe suggest that these candidate genes could be potential prognostic biomarkers of BCa and that they should be considered in the evaluation of clinical parameters of BCa.
APA, Harvard, Vancouver, ISO, and other styles
3

Herrero-Gonzalez, Sandra, and Antonio Di Cristofano. "New Routes to Old Places: PIK3R1 and PIK3R2 Join PIK3CA and PTEN as Endometrial Cancer Genes." Cancer Discovery 1, no. 2 (July 2011): 106–7. http://dx.doi.org/10.1158/2159-8290.cd-11-0116.

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

Vallejo-Díaz, Jesús, Monica Chagoyen, Manuel Olazabal-Morán, Ana González-García, and Ana Clara Carrera. "The Opposing Roles of PIK3R1/p85α and PIK3R2/p85β in Cancer." Trends in Cancer 5, no. 4 (April 2019): 233–44. http://dx.doi.org/10.1016/j.trecan.2019.02.009.

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

Yazdani, Reza, Zahra Hamidi, Fateme Babaha, Gholamreza Azizi, Saba Fekrvand, Hassan Abolhassani, and Asghar Aghamohammadi. "PIK3R1 Mutation Associated with Hyper IgM (APDS2 Syndrome): A Case Report and Review of the Literature." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 7 (October 11, 2019): 941–58. http://dx.doi.org/10.2174/1871530319666190225114739.

Full text
Abstract:
Background and Objective: APDS [Activated phosphoinositide 3-kinase (PI3K) δ Syndrome] is a newly found special form of primary immunodeficiency caused by mutations in genes encoding PI3Kδ subunits and over-activation of the PI3K signaling pathway. Gain-of-function and loss-of-function mutations in PIK3CD (encoding P110δ) and PIK3R1 (encoding p85α, p55α and p50α) lead to APDS1 and APDS2, respectively. The subsequent irregular PI3K downstream signaling cascade is associated with abnormalities in B cells and T cells and the consequent heterogeneous clinical manifestations including respiratory tract infections, autoimmunity, lymphoproliferation and not to mention primary antibody deficiency. In this study, we report a 12-year-old girl with a mutation in the PIK3R1 gene who manifested immunological phenotypes resembling hyper IgM syndrome along with a review of the literature of the previously reported patients. Methods: Whole exome sequencing was performed to detect the underlying genetic mutation in this patient. Results: A de novo heterozygous splice site mutation in the hot spot of the PIK3R1 gene within the intron 10 was found (c.1425+1G>A). Conclusion: Further investigations are required for evaluation of the underlying genetic defects and the possible associations between genetic underpinning and heterogeneous severity and features of the disease.
APA, Harvard, Vancouver, ISO, and other styles
6

Thorpe, Lauren M., Jennifer M. Spangle, Carolynn E. Ohlson, Hailing Cheng, Thomas M. Roberts, Lewis C. Cantley, and Jean J. Zhao. "PI3K-p110α mediates the oncogenic activity induced by loss of the novel tumor suppressor PI3K-p85α." Proceedings of the National Academy of Sciences 114, no. 27 (June 19, 2017): 7095–100. http://dx.doi.org/10.1073/pnas.1704706114.

Full text
Abstract:
Mutation or loss of the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K) is emerging as a transforming factor in cancer, but the mechanism of transformation has been controversial. Here we find that hemizygous deletion of the PIK3R1 gene encoding p85α is a frequent event in breast cancer, with PIK3R1 expression significantly reduced in breast tumors. PIK3R1 knockdown transforms human mammary epithelial cells, and genetic ablation of Pik3r1 accelerates a mouse model of HER2/neu-driven breast cancer. We demonstrate that partial loss of p85α increases the amount of p110α–p85 heterodimers bound to active receptors, augmenting PI3K signaling and oncogenic transformation. Pan-PI3K and p110α-selective pharmacological inhibition effectively blocks transformation driven by partial p85α loss both in vitro and in vivo. Together, our data suggest that p85α plays a tumor-suppressive role in transformation, and suggest that p110α-selective therapeutics may be effective in the treatment of breast cancer patients with PIK3R1 loss.
APA, Harvard, Vancouver, ISO, and other styles
7

Shi, Ting, Xiongjie Shen, and Ge Gao. "Gene Expression Profiles of Peripheral Blood Monocytes in Osteoarthritis and Analysis of Differentially Expressed Genes." BioMed Research International 2019 (November 26, 2019): 1–12. http://dx.doi.org/10.1155/2019/4291689.

Full text
Abstract:
Background. There is little understanding of the molecular processes involved in the pathogenesis of osteoarthritis, limiting early diagnosis and effective treatment of OA. Use of genechips can provide insights into the molecular pathogenesis of diseases. In this study, determination of gene expression profiles of osteoarthritis peripheral blood mononuclear cells will allow exploration of the molecular pathogenesis of OA and find out more candidate biomarkers and potential drug targets of OA. Result. A total of 1231 DEGs were screened out including 791 upregulated DEGs and 440 downregulated DEGs. The most significant upregulated DEG was RPL38, which may inhibit chondrocyte differentiation and synthesis of the extracellular matrix. PIK3CA, PIK3CB, PIK3CD, PIK3R1, MAPK14, IL1A, JUND, FOSL2, and PPP3CA were the gene symbols of the osteoclast differentiation pathway which was the most significant pathway enriched by DEGs. However, the MAPK signaling pathway occupied the core position of all the pathways which can regulate apoptosis, cell cycle, wnt signaling pathway, p53 signaling pathway, and phosphatidylinositol signaling system. Furthermore, PI3Ks may regulate IL1A, JUND, FOSL2 and PPP3CA through the MAPK signaling pathway. Conclusion. These identified DEGs and pathways may be novel biomarkers to monitor the changes of OA and can be a potential drug target for the treatment of OA.
APA, Harvard, Vancouver, ISO, and other styles
8

Cobleigh, Melody A., and Abde M. Abukhdeir. "Binimetinib activity in PIK3R1-mutant patient-derived xenografts (PDX) implanted into immunodeficient mice." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e13062-e13062. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e13062.

Full text
Abstract:
e13062 Background: The PIK3R1 gene is genetically altered in ̃3% of breast cancers in the Western and ̃17% in the Eastern worlds. We recently reported that breast cancer cells lacking protein expression of PIK3R1 had elevated levels of activated MEK, sensitizing them to the MEK inhibitor trametinib. To better understand whether MEK inhibition is a therapeutic option for breast cancer patients with mutated PIK3R1, we tested the newer generation MEK inhibitor, binimetinib, in a PDX mouse model. Methods: Two PDx models (table) were tested in athymic nude-foxn1nu (immune-compromised) mice. Both patients had had metastatic, grade 3 breast cancer and expressed moderate RNA levels of PIK3R1. Results: Body weights of treatment arms were unchanged throughout the experiment. The TNBC PDx study was halted early at 13 days because tumors reached the predefined maximum size of 1500 mm2. The binimetinib treated mice experienced slowed tumor growth (522.8 +/- 172.8%) compared to the vehicle control (720.7 +/- 229.1%), (p=0.0693). In the HR+ PDx model, the combination of binimetinib plus tamoxifen resulted in a statistically significant decrease (371.5 +/- 108.1%) in tumor volume compared to tamoxifen alone (525.0 +/- 154.1%; p = 0.0302). Conclusions: Our previous and current results suggest that mutation in PIK3R1 sensitizes cells to MEK inhibitors. Binimetinib inhibited growth in both models. This inhibition was of borderline significance in the TNBC model and was statistically significant in the ER+, HER2- model. To the best of our knowledge, these results provide the first evidence of binimetinib efficacy in PIK3R1-mutant, HR+, HER2- PDX immunodeficient mice. Plans for a phase II trial in patients with PIK3R1-mutant, HR+, HER2- breast cancer are underway.[Table: see text]
APA, Harvard, Vancouver, ISO, and other styles
9

Calixto-Hope, Lucas, Julieann Lee, Emily Sloan, Jeffrey Hofmann, Jessica Van Ziffle, Courtney Onodera, James Grenert, et al. "PATH-38. ROSETTE-FORMING GLIONEURONAL TUMOR IS DEFINED BY FGFR1 ACTIVATING ALTERATIONS WITH FREQUENT ACCOMPANYING PI3K AND MAPK PATHWAY MUTATIONS." Neuro-Oncology 21, Supplement_6 (November 2019): vi151—vi152. http://dx.doi.org/10.1093/neuonc/noz175.634.

Full text
Abstract:
Abstract BACKGROUND Rosette-forming glioneuronal tumor (RGNT) is an uncommon CNS tumor originally described in the fourth ventricle characterized by a low-grade glial neoplasm admixed with a rosette-forming neurocytic component. METHODS We reviewed clinicopathologic features of 42 patients with RGNT. Targeted next-generation sequencing was performed, and genome-wide methylation profiling is underway. RESULTS The 20 male and 22 female patients had a mean age of 25 years (range 3–47) at time of diagnosis. Tumors were located within or adjacent to the lateral ventricle (n=16), fourth ventricle (15), third ventricle (9), and spinal cord (2). All 31 tumors assessed to date contained FGFR1 activating alterations, either in-frame gene fusion, kinase domain tandem duplication, or hotspot missense mutation in the kinase domain (p.N546 or p.K656). While 7 of these 31 tumors harbored FGFR1 alterations as the solitary pathogenic event, 24 contained additional pathogenic alterations within PI3-kinase or MAP kinase pathway genes: 5 with additional PIK3CA and NF1 mutations, 4 with PIK3CA mutation, 3 with PIK3R1 mutation (one of which also contained focal RAF1 amplification), 5 with PTPN11 mutation (one with additional PIK3R1 mutation), and 2 with NF1 deletion. The other 5 cases demonstrated anaplastic features including hypercellularity and increased mitotic activity. Among these anaplastic cases, 3 harbored inactivating ATRX mutations and two harbored CDKN2A homozygous deletion, in addition to the FGFR1 alterations plus other PI3-kinase and MAP kinase gene mutations seen in those RGNT without anaplasia. CONCLUSION Independent of ventricular location, RGNT is defined by FGFR1 activating mutations or rearrangements, which are frequently accompanied by mutations involving PIK3CA, PIK3R1, PTPN11, NF1, and KRAS. Whereas pilocytic astrocytoma and ganglioglioma are characterized by solitary activating MAP kinase pathway alterations (e.g. BRAF fusion or mutation), RGNT are genetically more complex with dual PI3K-Akt-mTOR and Ras-Raf-MAPK pathway activation. Rare anaplastic examples may show additional ATRX and/or CDKN2A inactivation.
APA, Harvard, Vancouver, ISO, and other styles
10

Goodwin, Charles B., Zhenyun Yang, Sasidhar Vemula, Fuqin Yin, Reuben Kapur, and Rebecca J. Chan. "Genetic Disruption of the PI3K Regulatory Subunit, p85α Partially Normalizes Gain-of-Function PTPN11-Induced Hypersensitivity to GM-CSF in Hematopoietic Progenitors." Blood 114, no. 22 (November 20, 2009): 3968. http://dx.doi.org/10.1182/blood.v114.22.3968.3968.

Full text
Abstract:
Abstract Abstract 3968 Poster Board III-904 Juvenile Myelomonocytic Leukemia (JMML) is a lethal myeloproliferative disorder (MPD) of children, characterized by hyperproliferation of myelomonocytic cells and hypersensitivity to Granulocyte-Monocyte Colony-Stimulating Factor (GM-CSF). Most patients show hyperactivation of Ras via one or more mutations, including in the PTPN11 gene, which encodes the protein tyrosine phosphatase, Shp2. It has been demonstrated that gain-of-function mutant Shp2 (Shp2 E76K and Shp2 D61Y) causes hyperactivation of the Mitogen-Activated Protein Kinase (MAPK) pathway. Additionally, we have previously shown that macrophage progenitor cells transduced with Shp2 D61Y or Shp2 E76K showed elevated levels of phospho-Akt, both at baseline and following 1 hour of GM-CSF stimulation, indicating a role for the Phospho-Inositol-3-Kinase (PI3K)/Akt pathway in the phenotype of elevated proliferation and survival in mutant Shp2-expressing cells (Yang, et al, 2008). However, it remains to be elucidated how PI3K contributes to the phenotype of increased proliferation and survival in cells bearing gain-of-function mutations in Shp2. Class IA PI3K is a lipid kinase heterodimer consisting of one of three catalytic subunits (p110α, p110β, or p110δ) and one of two regulatory subunits (p85α or p85β). It has been demonstrated that knocking out the main regulatory subunit, p85α, abrogated the hyperproliferative phenotype in mast cell progenitors bearing an oncogenic mutation in Kit in a model of another MPD, Systemic Mastocytosis (Munugalavadla, et al, 2007). In order to examine whether eliminating expression of p85α would cause a similar correction in cells expressing gain-of-function mutant Shp2, we performed timed matings of mice heterozygous for the knock-out of Pik3r1, which encodes the p85α subunit as well as its isoforms, p55α and p50α, since homozygous Pik3r1-/- is lethal in utero. WT and Pik3r1-/- fetal liver cells were isolated from 14.5 day embryos and transduced with either WT Shp2 or mutant Shp2 E76K. Transduced cells were subjected to serum deprivation followed by a 24-hour treatment with increasing doses of GM-CSF, and proliferation was then measured with H3-thymidine incorporation assays. We found that the absence of all the Pik3r1 isoforms resulted in a significant but incomplete correction of GM-CSF hypersensitivity in Shp2 E76K-expressing cells. To further investigate this observation, WT Pik3r1 and Pik3r1-/- macrophage progenitors, transduced with WT Shp2 or mutant Shp2 E76K as described above, were serum- and growth factor-deprived and then stimulated for 1 hour with GM-CSF. Western blot analysis showed that there was an expected increase in phospho-Akt in WT Pik3r1 cells following GM-CSF stimulation and that this increase was larger in Shp2 E76K-expressing cells than in WT Shp2-expressing cells, as previously observed. Upon genetic disruption of Pik3r1, Akt activation was reduced in both WT Shp2- and Shp2 E76K-expressing cells; however, the phospho-Akt in the Shp2 E76K-expressing cells was not reduced to WT levels. The phospho-Akt levels mirrored the proliferation pattern displayed by these cells in the H3-thymidine incorporation assays, where a modest reduction in proliferation in Pik3r1-/-, Shp2 E76K cells corresponded to the modest reduction in phospho-Akt levels in the same cells. Additionally, we found that Pik3r1-/-, Shp2 E76K cells also showed a blunted increase in phospho-Erk levels following GM-CSF stimulation compared to the WT Pik3r1, Shp2 E76K cells, indicating that knocking out Pik3r1 affects the MAPK pathway as well, which likely also contributes to the reduction in proliferation seen in Pik3r1-/-, Shp2 E76K cells following GM-CSF stimulation. Based on these data, we conclude that: (1) gain-of-function Shp2 activity results in dysregulated PI3K signaling, contributing to the leukemic phenotype of increased proliferation and survival; (2) PI3K signaling is reduced but not completely normalized in the absence of the main regulatory subunit, p85α and its isoforms, in gain-of-function mutant Shp2-expressing cells; and (3) there is cross-talk between the PI3K and MAPK pathways in the presence of Shp2 activating mutations, which is revealed by knocking out Pik3r1. Disclosures: No relevant conflicts of interest to declare.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "PIK3R1"

1

Cizkova, Magdalena. "Pronostic and Predictive Markers in Breast Cancer - PI3K Signaling Pathway." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T021.

Full text
Abstract:
Les résultats des projets actuels apportent une information, sur différents aspects des rôles de la voie PI3K, dans le développement du cancer du sein, et la réponse au traitement. Les projets particuliers couvrent des sujets liés à la voie aux niveaux concernant les récepteurs de la famille HER, activant la voie PI3K, ainsi que PI3K et les effecteurs en découlant. Les effets pronostic et prédictif de la dérégulation de PI3K sont les sujets centraux de la recherche décrite ici. Une baisse d’expression de PI3KR1 est associée à une survie réduite dans notre cohorte de patients. Une attention particulière a été portée aux mutations de PIK3CA communes dans le cancer du sein. Tandis que les mutations de PIK3CA agissent comme des marqueurs de bon pronostic chez les patients anti-HER2-naïfs, ces mutations agissent au contraire comme prédicteurs négatifs de la réponse au traitement par trastuzumab. Les résultats décrits mènent un peu plus vers l’implication de plusieurs voies moléculaires altérées, en particulier la voie de signalisation Wnt, dans la tumorigénèse des cancers du sein PIK3CA mutés. De plus, nous avons testé les taux de lapatinib plasmatique montrant une augmentation pertinente dans les périodes d’état d’équilibre du traitement. Par ailleurs, nous avons démontré des incohérences dans l’évaluation de l’EGFR et proposé des approches pour l’interprétation des comptages d’immunohistochimie et de FISH. Tous ces sujets sont connectés par la 170 voie PI3K, et le besoin d’approfondir les connaissances actuelles, et d’apporter de nouvelles informations utiles applicables dans le futur dans les pratiques cliniques
Results of the presented research projects bring information about several aspects of the PI3K signaling pathway roles in breast cancer development and treatment response. The particular projects covered the subjects connected with the signaling pathway, ranging from the HER family receptors activating the pathway, and PI3K to the downstream levels of signalisation. The prognostic and predictive effect of PI3K deregulation was the central subject of the described research. The decreased expression of PIK3R1 associated with reduced survival of our patients. A special focus was put on the PIK3CA mutations which are common in breast cancer. Whereas the PIK3CA mutations act as a good prognostic marker in patients non-treated with the HER2 inhibitors, these mutations predict a negative response to trastuzumab treatment. The described results, furthermore, draw attention to the role of several altered molecular signaling pathways in breast cancer development, especially to the Wnt signaling pathway. The lapatinib plasma levels showing the relevant increase in comparison with the already described efficient steady-state levels were also described in one of the projects. Moreover, various modifications to EGFR status assessment were compared and showed that EGFR FISH and IHC count interpretation depended significantly on method and thresholds used. All these subjects are connected by the PI3K pathway, the need to deepen current knowledge and bring new useful information applicable in future clinical practice
APA, Harvard, Vancouver, ISO, and other styles
2

Tomlinson, Patsy Roseanne. "Mechanistic investigation of genotype-phenotype correlations in PIK3R1-related diseases." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271188.

Full text
Abstract:
The PIK3R1 gene encodes three proteins - p85$\alpha$, p50$\alpha$ and p55$\alpha$ - that are regulatory subunits of Class IA phosphoinositide 3-kinases (PI3Ks). These regulatory subunits heterodimerise with one of three catalytic subunit isoforms, namely p110$\alpha$, p110$\beta$, or p110$\delta$. Class IA PI3Ks are critical enzymes involved in fundamental metabolic and mitogenic signalling pathways. This thesis describes the delineation of biochemical and molecular mechanisms whereby PIK3R1 mutations cause diverse disease phenotypes observed in SHORT syndrome (defined by Short stature, Hyperextensibility, Ocular depression, Rieger anomaly and Teething delay), the primary immunodeficiency Activated PI3K-$\delta$ Syndrome 2 (APDS2), and cancer. Initial studies of purified wildtype or mutant PI3K complexes, utilising a modified PI3K fluorescence polarisation lipid kinase assay, established that SHORT syndrome-associated p85$\alpha$ mutations impaired phosphotyrosine peptide-stimulated PI3K activity when heterodimerised with either of the Class IA catalytic subunit isoforms. Two cancer-associated mutations assessed using the same assay demonstrated differential effects on PI3K function, causing either basal activation or impaired phosphotyrosine peptide-stimulated PI3K activity. To examine the effect of SHORT syndrome-associated p85$\alpha$ mutations in insulin-responsive cell types, 3T3-L1 preadipocyte models with conditional overexpression of p85$\alpha$ Y657X or p85$\alpha$ R649W were generated. Doxycycline-induced overexpression of mutant p85$\alpha$ attenuated insulin-stimulated Akt phosphorylation due to reduced insulin-stimulated association of p85$\alpha$/p110$\alpha$ heterodimers with either IRS1 or IRS2. This in turn resulted in impaired downstream signalling as indicated by low adipogenic efficiency. Cells and tissues isolated from Pik3r1$^{WT/Y657X}$ knock-in mice also demonstrated decreased insulin-stimulated Akt phosphorylation. Observations from a system with endogenous expression of mutant p85$\alpha$ Y657X supported the results obtained in the 3T3-L1 p85$\alpha$ overexpression models. The final part of this thesis focussed on a PIK3R1 exon skipping mutant (p85$\alpha$ $\Delta$Ex11) that confers PI3K activation in lymphocytes and causes APDS2. APDS2 patients have an immune-restricted phenotype, even though the mutation occurs within the ubiquitously expressed PIK3R1. To investigate this phenomenon, the doxycycline-inducible system was used to model overexpression of p85$\alpha$ $\Delta$Ex11, as well as an activating p110$\alpha$ H1047R mutation associated with cancer, in 3T3-L1 preadipocytes. Surprisingly, given that APDS2 is not normally associated with metabolic or growth problems, high overexpression of p85$\alpha$ $\Delta$Ex11 severely attenuated insulin-stimulated Akt phosphorylation and adipocyte differentiation. There was also reduced insulin-stimulated recruitment of p110$\alpha$ to either IRS1 or IRS2, and impaired heterodimerisation of p85$\alpha$ $\Delta$Ex11 with p110$\alpha$. Collectively, the data presented in this thesis contributes to the developing knowledge of PIK3R1-related diseases. In particular, these studies provided novel insights into the biochemical and molecular mechanisms of SHORT syndrome-associated p85$\alpha$ mutations. Additionally, these data delivered further understanding of potential mechanisms underlying the immune-specific phenotype of APDS2 caused by PIK3R1 mutations.
APA, Harvard, Vancouver, ISO, and other styles
3

Clayton, Zachary. "The Role of Pik3r1 in the Regulation of Adipose Tissue Insulin Sensitivity." Thesis, University of Oregon, 2018. http://hdl.handle.net/1794/23757.

Full text
Abstract:
Obesity is a burgeoning health crisis in the United States. Obesity is associated with an earlier and greater risk for developing metabolic diseases. Insulin resistance is a central and defining feature of the metabolic diseases associated with obesity. Class 1a Phosphatidylinositol 3-kinase (PI3K) is integral in canonical insulin signaling. PI3K contains regulatory (p85/, p55/, p50) and catalytic (p110//) subunits. The regulatory subunits are encoded by Pik3r1. Increased Pik3r1 abundance has been observed in obese white adipose tissue (WAT). Furthermore, obese mice with heterozygous (HZ) knockout of Pik3r1 remain insulin sensitive, despite marked obesity. Taken together, it is crucial to understand the role of WAT Pik3r1 in regulating insulin sensitivity. Recently, literature has demonstrated that standard vivarium temperature (~22C) is a thermal stress for mice, as their thermoneutral zone is ~30C. Considering mice are a preclinical model for studying metabolic disease, it is critical to understand cellular and systemic responses to high fat diet (HFD) at 22C and 30C. To determine the role of AT Pik3r1 in regulating insulin sensitivity, mice with constitutive and inducible adipocyte specific hetero/homozygous knockout of Pik3r1 were studied following acute (three days) and chronic (12 week) HFD, respectively. Furthermore, insulin sensitivity was assessed in mice with adipocyte specific overexpression (OX) of p55. To determine the influence of short-term (8 and 12 days) thermoneutral housing on insulin sensitivity, mice were studied following one and five days of HFD at 22C and 30C (one week acclimation at 30C prior to starting HFD). Visceral WAT p85 abundance was increased (2-fold) following acute HFD in wild-type mice, with a parallel increase in systemic insulin resistance. HZ knockout of adipocyte Pik3r1 prevented acute HFD induced systemic insulin resistance. Furthermore, HZ knockout of adipocyte Pik3r1 reversed obesity induced glucose intolerance and enhanced systemic insulin sensitivity and adipocyte insulin signaling. Moreover, OX of adipocyte p55 enhanced (40%) glucose tolerance, energy expenditure (30%: light cycle; 45%: dark cycle) and markers of AT thermogenesis in brown AT. Lastly, housing temperature had a significant impact on the cellular pathways that regulate glucose metabolism in response to HFD exposure. This dissertation includes previously published co-authored material.
APA, Harvard, Vancouver, ISO, and other styles
4

Behrmann, Christoph [Verfasser], Hubert [Gutachter] Kübler, and Ralf C. [Gutachter] Bargou. "MicroRNA-221 sensitiviert Prostatakarzinomzellen gegenüber TRAIL durch Inhibition von SOCS-3 und PIK3R1 / Christoph Behrmann ; Gutachter: Hubert Kübler, Ralf C. Bargou." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1204006334/34.

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

Behrmann, Christoph Verfasser], Hubert [Gutachter] Kübler, and Ralf C. [Gutachter] [Bargou. "MicroRNA-221 sensitiviert Prostatakarzinomzellen gegenüber TRAIL durch Inhibition von SOCS-3 und PIK3R1 / Christoph Behrmann ; Gutachter: Hubert Kübler, Ralf C. Bargou." Würzburg : Universität Würzburg, 2020. http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-199205.

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

Nilsson, Ardnor Sofie. "Genetic studies of stroke in Northern Sweden." Doctoral thesis, Umeå : Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-887.

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

Reinhardt, Kristin [Verfasser]. "Prävalenz von PIK3CA-Genmutationen beim Mammakarzinom / Kristin Reinhardt." Halle, 2018. http://d-nb.info/1160514526/34.

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

Gebauer, Mirjam. "Wendekrisen der Pikaro im deutschen Roman der 1990er Jahre." Trier Wiss. Verl. Trier, 2003. http://deposit.ddb.de/cgi-bin/dokserv?id=2826307&prov=M&dok_var=1&dok_ext=htm.

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

Gebauer, Mirjam. "Wendekrisen der Pikaro im deutschen Roman der 1990er Jahre /." Trier : WVT, Wissenschaftlicher Verlag Trier, 2006. http://catalog.hathitrust.org/api/volumes/oclc/70840926.html.

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

Schacht, Hannes Verfasser], and Guido [Akademischer Betreuer] [Sauter. "PIK3CA-Amplifikationen in humanen Lungenkarzinomen / Hannes Schacht. Betreuer: Guido Sauter." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020465387/34.

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

Books on the topic "PIK3R1"

1

Gibran, Kahlil. Pikar. Lahore: Aina Adab, 1990.

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

Pikhre patte: Afsāne. Barlin: Rahbar Pablīkeshanz, 2008.

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

Samsudi. Babalik pikir. 2nd ed. Bandung: Kiblat Buku Utama, 2002.

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

Ataev, D. Du̇nĭă ve pikir. Ashgabat: Ylym, 1985.

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

Pikro karnavali: Poiēmata. Athēna: Psychogios, 2013.

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

Ta pikra glyka: Histories. Athēna: Metaichmio, 2008.

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

Danilov, L. V. Ri͡a︡dy Volʹterra-Pikara v teorii nelineĭnykh ėlektricheskikh t͡s︡epeĭ. Moskva: "Radio i svi͡a︡zʹ", 1987.

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

Sutrisno, Slamet. Budaya pikir "kawruh" Jawa: Laporan penelitian. Jogjakarta: Lembaga Penelitian, Universitas Gadjah Mada, Departemen Pendidikan Nasional, 2001.

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

Wendekrisen: Der Pikaro im deutschen Roman der 1990er Jahre. Trier: WVT, Wissenschaftlicher Verlag Trier, 2006.

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

Strobel, Katja. Wandern, Mäandern, Erzählen: Die Pikara als Grenzgängerin des Subjekts. München: Fink, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "PIK3R1"

1

Lougaris, Vassilios, and Alessandro Plebani. "PIK3R1 Deficiency-Associated Agammaglobulinemia." In Encyclopedia of Medical Immunology, 1–3. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-9209-2_19-1.

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

Lougaris, Vassilios, and Alessandro Plebani. "PIK3R1 Deficiency-Associated Agammaglobulinemia." In Encyclopedia of Medical Immunology, 535–37. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_19.

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

Park, Ben Ho. "PIK3CA." In Encyclopedia of Cancer, 2892–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4570.

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

Park, Ben Ho. "PIK3CA." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4570-3.

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

Park, Ben Ho. "PIK3CA." In Encyclopedia of Cancer, 3584–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4570.

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

Salajegheh, Ali. "PIK3R2 (p85β) – Phosphatidylinositol 3-Kinase β-Subunit." In Angiogenesis in Health, Disease and Malignancy, 245–51. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_38.

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

Conboy, Erin, James T. Bennett, and David Deyle. "PIK3CA-Related Overgrowth Spectrum (PROS)." In Evidence-Based Management of Head and Neck Vascular Anomalies, 285–96. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92306-2_33.

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

Velho, Sérgia, Carla Oliveira, and Raquel Seruca. "PIK3CA Gene Alterations in Human Cancers." In Bioinformatics in Cancer and Cancer Therapy, 1–20. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-576-3_10.

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

Salajegheh, Ali. "Phosphatidylinositol-4, 5-Bisphosphate 3-Kinase (PIK3Ca)." In Angiogenesis in Health, Disease and Malignancy, 241–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_37.

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

Samuels, Yardena, and Todd Waldman. "Oncogenic Mutations of PIK3CA in Human Cancers." In Current Topics in Microbiology and Immunology, 21–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_68.

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

Conference papers on the topic "PIK3R1"

1

Jaiswal, Bijay S., Vasantharajan Janakiraman, Subhra Chaudhuri, Howard M. Stern, Noelyn M. Kljavin, Weiru Wang, Zhengyan Kan, et al. "Abstract 305: Frequent PIK3R1 somatic mutations promote oncogenic signaling." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-305.

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

Abukhdeir, AM, SB Turturro, MS Najor, SS Brar, and MA Cobleigh. "Abstract P6-11-17: Mutations in PIK3R1 activate multiple pathways in breast cancer." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-11-17.

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

Kim, Jee Hung, Woo Sun Kwon, Won Suk Lee, Tae Soo Kim, Kyu Hyun Park, Jae Kyung Roh, Joong Bae Ahn, Hyun Cheol Chung, and Sun Young Rha. "Abstract 430: Novel biomarkers for VEGFR inhibitors in metastatic renal cell carcinoma: BIM expression, and germline polymorphisms of BIM and PIK3R1." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-430.

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

Kim, Chan, Woo Sun Kwon, Sun Young Rha, Sun Kyung Kang, Hyoki Kim, Carolyn Buser-Doepner, Li Yan, Rakesh Kumar, and Hyun Cheol Chung. "Abstract 4694: Whole-exome sequencing of gastric cancer identifies germline PIK3R1 variant as a novel genetic biomarker for a PI3K beta-isoform selective inhibitor, GSK2636771." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4694.

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

Laing, Lance, Salmaan Khan, Ian MacNeil, Catherine Kuzmicki, Samantha Kharbush, Benjamin Rich, Abhay Shukla Shukla, Kelly Brass Brass, and Brian Sullivan Sullivan. "Abstract P1-09-07: Sub-group of PIK3CA WT breast cancer patients have hyperactive S1P signaling tumor cells responsive to PIK3-inhibitors: Functional signaling profile test identifies new patient group who may benefit from PIK3-targeted therapies." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p1-09-07.

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

Cao, Z. Alexander, Maria Pinzon-Ortiz, Yan Chen, Xiaoyan Li, Pedro J. Beltran, Jennifer Gansert, Malte Peters, Robert Schlegel, Karl M. Schumacher, and Alan Huang. "Abstract 3683: Targeting PIK3CA mutant breast cancer with the combination of PIK3CA-specific inhibitor, BYL719, and IGF1-R antibody, ganitumab." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3683.

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

Niesen, J., J. Ohli, and U. Schüller. "PIK3CA mutations significantly enhance the growth of Shh medulloblastoma." In 31. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1645005.

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

Kim, Heesue. "Abstract 2109: PIK3CA mutations in hepatocellular carcinoma in Korea." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2109.

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

Aktas, B., S. Kasimir-Bauer, S. Kasper, C. Derks, R. Kimmig, M. Schuler, and M. Tewes. "P4-07-05: Comparison of PIK3CA Hot Spot Mutations in the Primary Tumor or Metastases with PIK3CA Mutations or PIK3CA Over-Expression in Circulating Tumor Cells of Metastatic Breast Cancer Patients under Sequential Palliative Therapy." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-07-05.

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

Keraite, Ieva, Virginia Alvarez-Garcia, Jurgen Del Favero, Maiwenn Kersaudy-Kerhoas, and Nicholas Leslie. "Abstract B55: PIK3CA mutation enrichment and detection in clinical samples." In Abstracts: AACR Special Conference on Advances in Liquid Biopsies; January 13-16, 2020; Miami, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.liqbiop20-b55.

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

Reports on the topic "PIK3R1"

1

Zhao, Jean J. Targeting Breast Cancers Featuring Activating Mutations in PIK3CA by Generating a Lethal Dose of PIP3. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada485346.

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

Zhao, Jean J. Targeting Breast Cancers Featuring Activating Mutations in PIK3CA by Generating a Lethal Dose of PIP3. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada506562.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'PIK3R1' 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