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https://www.readbyqxmd.com/read/29603734/school-based-physical-therapy-services-and-student-functional-performance-at-school
#1
Sarah Westcott Mccoy, Susan K Effgen, Lisa A Chiarello, Lynn M Jeffries, Alejandro G Villasante Tezanos
AIM: We explored relationships of school-based physical therapy to standardized outcomes of students receiving physical therapy. METHOD: Using a practice-based evidence research design, School Function Assessment (SFA) outcomes of 296 students with disabilities (mean age 7y 4mo [standard deviation 2y]; 166 males, 130 females), served by 109 physical therapists, were explored. After training, therapists completed 10 SFA scales on students at the beginning and end of the school year...
March 30, 2018: Developmental Medicine and Child Neurology
https://www.readbyqxmd.com/read/29600476/percutaneous-transhepatic-intrahepatic-portosystemic-shunt-for-variceal-bleeding-with-chronic-portal-vein-occlusion-after-splenectomy
#2
Junyang Luo, Mingan Li, Youyong Zhang, Haofan Wang, Mingsheng Huang, Zhengran Li, Junwei Chen, Chun Wu, Jiesheng Qian, Shouhai Guan, Zaibo Jiang
OBJECTIVES: The purpose of this study was to introduce a modified transjugular intrahepatic portosystemic shunt (TIPS), a percutaneous transhepatic intrahepatic portosystemic shunt (PTIPS), and to evaluate its feasibility and efficacy in patients with variceal bleeding with chronic portal vein occlusion (CPVO) after splenectomy. METHODS: Twenty-four cirrhotic patients with CPVO after splenectomy who received PTIPS between 2010 and 2015 were included in this retrospective study...
March 29, 2018: European Radiology
https://www.readbyqxmd.com/read/29190394/acetylation-of-53bp1-dictates-the-dna-double-strand-break-repair-pathway
#3
Xiang Guo, Yongtai Bai, Meimei Zhao, Mei Zhou, Qinjian Shen, Cai-Hong Yun, Hongquan Zhang, Wei-Guo Zhu, Jiadong Wang
P53-binding protein 1 (53BP1) plays critical roles in DNA double strand break (DSB) repair by promoting non-homologous end joining (NHEJ), and loss of 53BP1 abolishes PARPi sensitivity in BRCA1-deficient cells by restoring homologous recombination (HR). 53BP1 is one of the proteins initially recruited to sites of DSBs via recognition of H4K20me2 through the Tudor-UDR domain and H2AK15ub through the UDR motif. Although extensive studies have been conducted, it remains unclear how the post-translational modification of 53BP1 affects DSB repair pathway choice...
January 25, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29078319/ptip-chromatin-regulator-controls-development-and-activation-of-b-cell-subsets-to-license-humoral-immunity-in-mice
#4
Dan Su, Stijn Vanhee, Rebeca Soria, Elin Jaensson Gyllenbäck, Linda M Starnes, Martina Kubec Højfeldt, Gabriel K Pedersen, Joan Yuan, Jeremy A Daniel
B cell receptor signaling and downstream NF-κB activity are crucial for the maturation and functionality of all major B cell subsets, yet the molecular players in these signaling events are not fully understood. Here we use several genetically modified mouse models to demonstrate that expression of the multifunctional BRCT (BRCA1 C-terminal) domain-containing PTIP (Pax transactivation domain-interacting protein) chromatin regulator is controlled by B cell activation and potentiates steady-state and postimmune antibody production in vivo...
October 31, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29038466/replication-fork-reversal-triggers-fork-degradation-in-brca2-defective-cells
#5
Sofija Mijic, Ralph Zellweger, Nagaraja Chappidi, Matteo Berti, Kurt Jacobs, Karun Mutreja, Sebastian Ursich, Arnab Ray Chaudhuri, Andre Nussenzweig, Pavel Janscak, Massimo Lopes
Besides its role in homologous recombination, the tumor suppressor BRCA2 protects stalled replication forks from nucleolytic degradation. Defective fork stability contributes to chemotherapeutic sensitivity of BRCA2-defective tumors by yet-elusive mechanisms. Using DNA fiber spreading and direct visualization of replication intermediates, we report that reversed replication forks are entry points for fork degradation in BRCA2-defective cells. Besides MRE11 and PTIP, we show that RAD52 promotes stalled fork degradation and chromosomal breakage in BRCA2-defective cells...
October 16, 2017: Nature Communications
https://www.readbyqxmd.com/read/28976802/the-mixed-lineage-leukemia-4-mll4-methyltransferase-complex-is-involved-in-transforming-growth-factor-beta-tgf-%C3%AE-activated-gene-transcription
#6
Roy Baas, Hetty A A M van Teeffelen, Sjoerd J D Tjalsma, H Th Marc Timmers
Sma and Mad related (SMAD)-mediated Transforming Growth Factor β (TGF-β) and Bone Morphogenetic Protein (BMP) signaling is required for various cellular processes. The activated heterotrimeric SMAD protein complexes associate with nuclear proteins such as the histone acetyltransferases p300, PCAF and the Mixed Lineage Leukemia 4 (MLL4) subunit Pax Transactivation domain-Interacting Protein (PTIP) to regulate gene transcription. We investigated the functional role of PTIP and PTIP Interacting protein 1 (PA1) in relation to TGF-β-activated SMAD signaling...
2018: Transcription
https://www.readbyqxmd.com/read/28938547/ptip-promotes-recurrence-and-metastasis-of-hepatocellular-carcinoma-by-regulating-epithelial-mesenchymal-transition
#7
Shusheng Leng, Mingyang Yang, Yanhua Zhao, Jingfeng Zhao, Zhijun Zeng, Yunpeng Yang, Jiatian Yuan, Bo Lv, Fan Jun, Bing Wang
Hepatocellular carcinoma (HCC) is one of the most lethal tumors worldwide, which is mainly due to the high recurrence and metastasis rate after hepatectomy. In this study, we found that PTIP expression was dramatically upregulated in human HCC tissues and cell lines. High expression of PTIP was shown to be associated with aggressive clinicopathological features, including liver cirrhosis, vascular invasion and advanced stage. In addition, PTIP overexpression was independently associated with shorter survival and increased HCC recurrence in patients...
August 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/28669924/histone-h3-lysine-4-methyltransferase-kmt2d
#8
REVIEW
Eugene Froimchuk, Younghoon Jang, Kai Ge
Histone-lysine N-methyltransferase 2D (KMT2D), also known as MLL4 and MLL2 in humans and Mll4 in mice, belongs to a family of mammalian histone H3 lysine 4 (H3K4) methyltransferases. It is a large protein over 5500 amino acids in size and is partially functionally redundant with KMT2C. KMT2D is widely expressed in adult tissues and is essential for early embryonic development. The C-terminal SET domain is responsible for its H3K4 methyltransferase activity and is necessary for maintaining KMT2D protein stability in cells...
September 5, 2017: Gene
https://www.readbyqxmd.com/read/28475402/dna-repair-genes-paxip1-and-tp53bp1-expression-is-associated-with-breast-cancer-prognosis
#9
Giuliana De Gregoriis, Juliene Antonio Ramos, Priscila Valverde Fernandes, Giselle Maria Vignal, Rafael Canfield Brianese, Dirce Maria Carraro, Alvaro N Monteiro, Claudio José Struchiner, Guilherme Suarez-Kurtz, Rosane Vianna-Jorge, Marcelo Alex de Carvalho
Despite remarkable advances in diagnosis, prognosis and treatment, advanced or recurrent breast tumors have limited therapeutic approaches. Many treatment strategies try to explore the limitations of DNA damage response (DDR) in tumor cells to selectively eliminate them. BRCT (BRCA1 C-terminal) domains are present in a superfamily of proteins involved in cell cycle checkpoints and the DDR. Tandem BRCT domains (tBRCT) represent a distinct class of these domains. We investigated the expression profile of 7 tBRCT genes (BARD1, BRCA1, LIG4, ECT2, MDC1, PAXIP1/PTIP and TP53BP1) in breast cancer specimens and observed a high correlation between PAXIP1 and TP53BP1 gene expression in tumor samples...
June 3, 2017: Cancer Biology & Therapy
https://www.readbyqxmd.com/read/28415612/ptip-promotes-recurrence-and-metastasis-of-hepatocellular-carcinoma-by-regulating-epithelial-mesenchymal-transition
#10
Shusheng Leng, Mingyang Yang, Yanhua Zhao, Jingfeng Zhao, Zhijun Zeng, Yunpeng Yang, Jiatian Yuan, Bo Lv, Fan Jun, Bing Wang
Hepatocellular carcinoma (HCC) is one of the most lethal tumors worldwide, which is mainly due to the high recurrence and metastasis rate after hepatectomy. In this study, we found that PTIP expression was dramatically upregulated in human HCC tissues and cell lines. High expression of PTIP was shown to be associated with aggressive clinicopathological features, including liver cirrhosis, vascular invasion and advanced stage. In addition, PTIP overexpression was independently associated with shorter survival and increased HCC recurrence in patients...
March 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28272113/multidisciplinary-mentoring-programs-to-enhance-junior-faculty-research-grant-success
#11
Stephanie A Freel, Paige C Smith, Ebony N Burns, Joanna B Downer, Ann J Brown, Mark W Dewhirst
PROBLEM: Junior faculty face challenges in establishing independent research careers. Declining funding combined with a shift to multidisciplinary, collaborative science necessitates new mentorship models and enhanced institutional support. APPROACH: Two multidisciplinary mentorship programs to promote grant success for junior faculty were established at the Duke University School of Medicine beginning in 2011. These four-month programs-the Path to Independence Program (PtIP) for National Institutes of Health (NIH) R applicants and the K Club for NIH K applicants-use multiple senior faculty mentors and professional grant-writing staff to provide a 20-hour joint curriculum comprising a series of lectures, hands-on workshops, career development counseling, peer groups, and an internal study section...
October 2017: Academic Medicine: Journal of the Association of American Medical Colleges
https://www.readbyqxmd.com/read/28213517/the-p53-binding-protein-1-tudor-interacting-repair-regulator-complex-participates-in-the-dna-damage-response
#12
Aili Zhang, Bo Peng, Ping Huang, Junjie Chen, Zihua Gong
The 53BP1-dependent end-joining pathway plays a critical role in double strand break repair and is uniquely responsible for cellular sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi) in BRCA1-deficient cancers. We and others have investigated the downstream effectors of 53BP1, including replication timing regulatory factor 1 (RIF1) and Pax transactivation domain-interacting protein (PTIP), in the past few years to elucidate how loss of the 53BP1-dependent repair pathway results in PARPi resistance in BRCA1 patients...
April 21, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27474475/ptip-loss-protects-brca-deficient-cells-from-dna-damage-and-cell-death
#13
LETTER
(no author information available yet)
Replication fork protection reduces chemosensitivity in BRCA-deficient cells without restoring HR.
September 2016: Cancer Discovery
https://www.readbyqxmd.com/read/27443740/replication-fork-stability-confers-chemoresistance-in-brca-deficient-cells
#14
Arnab Ray Chaudhuri, Elsa Callen, Xia Ding, Ewa Gogola, Alexandra A Duarte, Ji-Eun Lee, Nancy Wong, Vanessa Lafarga, Jennifer A Calvo, Nicholas J Panzarino, Sam John, Amanda Day, Anna Vidal Crespo, Binghui Shen, Linda M Starnes, Julian R de Ruiter, Jeremy A Daniel, Panagiotis A Konstantinopoulos, David Cortez, Sharon B Cantor, Oscar Fernandez-Capetillo, Kai Ge, Jos Jonkers, Sven Rottenberg, Shyam K Sharan, André Nussenzweig
Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors. Here we show that loss of the MLL3/4 complex protein, PTIP, protects Brca1/2-deficient cells from DNA damage and rescues the lethality of Brca2-deficient embryonic stem cells. However, PTIP deficiency does not restore homologous recombination activity at double-strand breaks...
July 21, 2016: Nature
https://www.readbyqxmd.com/read/27318548/long-term-functional-outcomes-after-penoscrotal-hypospadias-repair-a-retrospective-comparative-study-of-proximal-tip-onlay-and-duckett
#15
COMPARATIVE STUDY
Pierre-Alain Hueber, Monica Salgado Diaz, Yann Chaussy, Julie Franc-Guimond, Diego Barrieras, Anne-Marie Houle
INTRODUCTION: A variety of techniques are available for proximal hypospadias repair. Onlay, proximal tubularized incised plate (TIP), and Duckett are among the popular choices because they can be performed as a one-step procedure. However, the decision to select a procedure often comes down to the surgeon's preference rather than that supported by evidence-based data. In particular, there is a paucity of literature on the long-term urinary outcomes after proximal hypospadias repair. OBJECTIVE: The aim of this study was to evaluate the evolution of long-term uroflowmetry parameters after proximal hypospadias surgery over a long-term follow-up including the adolescent period...
August 2016: Journal of Pediatric Urology
https://www.readbyqxmd.com/read/26744420/a-ptip-pa1-subcomplex-promotes-transcription-for-igh-class-switching-independently-from-the-associated-mll3-mll4-methyltransferase-complex
#16
Linda M Starnes, Dan Su, Laura M Pikkupeura, Brian T Weinert, Margarida A Santos, Andreas Mund, Rebeca Soria, Young-Wook Cho, Irina Pozdnyakova, Martina Kubec Højfeldt, Andrea Vala, Wenjing Yang, Blanca López-Méndez, Ji-Eun Lee, Weiqun Peng, Joan Yuan, Kai Ge, Guillermo Montoya, André Nussenzweig, Chunaram Choudhary, Jeremy A Daniel
Class switch recombination (CSR) diversifies antibodies for productive immune responses while maintaining stability of the B-cell genome. Transcription at the immunoglobulin heavy chain (Igh) locus targets CSR-associated DNA damage and is promoted by the BRCT domain-containing PTIP (Pax transactivation domain-interacting protein). Although PTIP is a unique component of the mixed-lineage leukemia 3 (MLL3)/MLL4 chromatin-modifying complex, the mechanisms for how PTIP promotes transcription remain unclear. Here we dissected the minimal structural requirements of PTIP and its different protein complexes using quantitative proteomics in primary lymphocytes...
January 15, 2016: Genes & Development
https://www.readbyqxmd.com/read/26368543/critical-function-of-%C3%AE-h2a-in-s-phase
#17
Eva Mejia-Ramirez, Oliver Limbo, Petra Langerak, Paul Russell
Phosphorylation of histone H2AX by ATM and ATR establishes a chromatin recruitment platform for DNA damage response proteins. Phospho-H2AX (γH2AX) has been most intensively studied in the context of DNA double-strand breaks caused by exogenous clastogens, but recent studies suggest that DNA replication stress also triggers formation of γH2A (ortholog of γH2AX) in Schizosaccharomyces pombe. Here, a focused genetic screen in fission yeast reveals that γH2A is critical when there are defects in Replication Factor C (RFC), which loads proliferating cell nuclear antigen (PCNA) clamp onto duplex DNA...
September 2015: PLoS Genetics
https://www.readbyqxmd.com/read/26001054/the-ptip-associated-histone-methyltransferase-complex-prevents-stress-induced-maladaptive-cardiac-remodeling
#18
Adam B Stein, Sascha N Goonewardena, Thomas A Jones, Parker J Prusick, Ahmad A Bazzi, Jane M Belyavskaya, Makayla M McCoskey, Rachel A Dandar
Pressure overload induces stress-induced signaling pathways and a coordinated transcriptional response that begets concentric cardiac hypertrophy. Although concentric hypertrophy initially attenuates wall stress and maintains cardiac function, continued stress can result in maladaptive cardiac remodeling. Cardiac remodeling is orchestrated by transcription factors that act within the context of an epigenetic landscape. Since the epigenetic landscape serves as a molecular link between environmental factors (stress) and cellular phenotype (disease), defining the role of the epigenome in the development and progression of cardiac remodeling could lead to new therapeutic approaches...
2015: PloS One
https://www.readbyqxmd.com/read/25799990/mad2l2-controls-dna-repair-at-telomeres-and-dna-breaks-by-inhibiting-5-end-resection
#19
Vera Boersma, Nathalie Moatti, Sandra Segura-Bayona, Marieke H Peuscher, Jaco van der Torre, Brigitte A Wevers, Alexandre Orthwein, Daniel Durocher, Jacqueline J L Jacobs
Appropriate repair of DNA lesions and the inhibition of DNA repair activities at telomeres are crucial to prevent genomic instability. By fuelling the generation of genetic alterations and by compromising cell viability, genomic instability is a driving force in cancer and ageing. Here we identify MAD2L2 (also known as MAD2B or REV7) through functional genetic screening as a novel factor controlling DNA repair activities at mammalian telomeres. We show that MAD2L2 accumulates at uncapped telomeres and promotes non-homologous end-joining (NHEJ)-mediated fusion of deprotected chromosome ends and genomic instability...
May 28, 2015: Nature
https://www.readbyqxmd.com/read/25631048/the-groucho-associated-phosphatase-ppm1b-displaces-pax-transactivation-domain-interacting-protein-ptip-to-switch-the-transcription-factor-pax2-from-a-transcriptional-activator-to-a-repressor
#20
Saji Abraham, Raghavendra Paknikar, Samina Bhumbra, Danny Luan, Rohan Garg, Gregory R Dressler, Sanjeevkumar R Patel
Pax genes encode developmental regulatory proteins that specify cell lineages and tissues in metazoans. Upon binding to DNA through the conserved paired domain, Pax proteins can recruit both activating and repressing complexes that imprint distinct patterns of histone methylation associated with either gene activation or silencing. How the switch from Pax-mediated activation to repression is regulated remains poorly understood. In this report, we identify the phosphatase PPM1B as an essential component of the Groucho4 repressor complex that is recruited by Pax2 to chromatin...
March 13, 2015: Journal of Biological Chemistry
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