A5103223399- DNA Repair Mechanisms
- RNA modifications and cancer
- Mitochondrial Function and Pathology
- Genetic Neurodegenerative Diseases
- RNA and protein synthesis mechanisms
- Identification and Quantification in Food
- RNA Research and Splicing
- CRISPR and Genetic Engineering
- Cancer-related gene regulation
- Ichthyology and Marine Biology
- Genetic factors in colorectal cancer
- DNA and Nucleic Acid Chemistry
- Pediatric health and respiratory diseases
- Asthma and respiratory diseases
- Fish Biology and Ecology Studies
- Invertebrate Immune Response Mechanisms
- Genetic diversity and population structure
- Muscle Physiology and Disorders
- Aquaculture disease management and microbiota
- PARP inhibition in cancer therapy
- Immune Response and Inflammation
- Cancer-related Molecular Pathways
- Advanced biosensing and bioanalysis techniques
- Diabetic Foot Ulcer Assessment and Management
- SARS-CoV-2 and COVID-19 Research
The University of Texas Medical Branch at Galveston
2015-2025
AbbVie (United States)
2022
Pharmacyclics (United States)
2022
University of Münster
2022
Nitte University
2017-2021
Ackerman Institute for the Family
2018
Rutgers, The State University of New Jersey
2018
Stanford University
2016-2018
Université de Toulouse
2014-2017
Université Toulouse III - Paul Sabatier
2014-2017
Abstract DNA double-strand breaks (DSBs) leading to loss of nucleotides in the transcribed region can be lethal. Classical non-homologous end-joining (C-NHEJ) is dominant pathway for DSB repair (DSBR) adult mammalian cells. Here we report that during such DSBR, C-NHEJ proteins form a multiprotein complex with RNA polymerase II and preferentially associate genes after induction. Depletion factors significantly abrogates DSBR but not non-transcribed genes. We hypothesized nascent serve as...
Ribosome is responsible for protein synthesis in all organisms and ribosomal proteins (RPs) play important roles the formation of a functional ribosome. L11 was recently shown to regulate p53 activity through direct binding with MDM2 abrogating MDM2-induced degradation response stress. However, studies were performed cell lines significance this tumor suppressor function has yet be explored animal models. To investigate effects deletion its physiological relevance activity, we knocked down...
How huntingtin (HTT) triggers neurotoxicity in Huntington’s disease (HD) remains unclear. We report that HTT forms a transcription-coupled DNA repair (TCR) complex with RNA polymerase II subunit A (POLR2A), ataxin-3, the enzyme polynucleotide-kinase-3'-phosphatase (PNKP), and cyclic AMP-response element-binding (CREB) protein (CBP). This senses facilitates damage during transcriptional elongation, but its functional integrity is impaired by mutant HTT. Abrogated PNKP activity results...
DNA strand-breaks (SBs) with non-ligatable ends are generated by ionizing radiation, oxidative stress, various chemotherapeutic agents, and also as base excision repair (BER) intermediates. Several neurological diseases have already been identified being due to a deficiency in end-processing activities. Two common dirty ends, 3’-P 5’-OH, processed mammalian polynucleotide kinase 3’-phosphatase (PNKP), bifunctional enzyme 5’-kinase We made the unexpected observation that PNKP stably...
Ribosomes are responsible for protein synthesis in all cells. Ribosomal S19 (RPS19) is one of the 79 ribosomal proteins (RPs) vertebrates. Heterozygous mutations RPS19 have been identified 25% patients with Diamond-Blackfan anemia (DBA), but relationship between and pure red-cell aplasia DBA unclear. In this study, we developed an RPS19-deficient zebrafish by knocking down rps19 using a Morpholino antisense oligo. The animals showed dramatic decrease blood cells as well deformities head tail...
Non-coding RNAs (ncRNAs) play key roles in diverse cellular activities, and efficient ncRNA function requires extensive posttranscriptional nucleotide modifications. Small nucleolar (snoRNAs) are a group of ncRNAs that guide the modification specific nucleotides ribosomal (rRNAs) small nuclear RNAs. To investigate physiological relevance rRNA vertebrates, we suppressed expression three snoRNAs (U26, U44 U78), either by disrupting host gene splicing or inhibiting snoRNA precursor processing,...
Why mammalian cells possess multiple DNA glycosylases (DGs) with overlapping substrate ranges for repairing oxidatively damaged bases via the base excision repair (BER) pathway is a long-standing question. To determine biological role of these DGs, null animal models have been generated. Here, we report generation and characterization mice lacking Neil2 (Nei-like 2). As in deficient each other four oxidized base-specific DGs (OGG1, NTH1, NEIL1, NEIL3), Neil2-null show no overt phenotype....
Infection with the Gram-negative, microaerophilic bacterium Helicobacter pylori induces an inflammatory response and oxidative DNA damage in gastric epithelial cells that can lead to cancer (GC). However, underlying pathogenic mechanism is largely unclear. Here, we report suppression of Nei-like glycosylase 2 (NEIL2), a mammalian specifically removes oxidized bases, one through which H. infection may fuel accumulation leading GC. Using cultured cell lines, biopsy specimens, primary cells,...
DNA damage repair genes are modifiers of disease onset in Huntington's (HD), but how this process intersects with associated pathways remains unclear. Here we evaluated the mechanistic contributions protein inhibitor activated STAT-1 (PIAS1) HD mice and patient-derived induced pluripotent stem cells (iPSCs) find a link between PIAS1 pathways. We show that is component transcription-coupled complex, includes end processing enzyme polynucleotide kinase-phosphatase (PNKP), SUMO E3 ligase for...
The Bruton’s tyrosine kinase (BTK) inhibitor ibrutinib irreversibly binds BTK at Cys 481 , inhibiting its activity and thus blocking transduction of B cell receptor (BCR) signaling. Although is durably effective in patients with malignancies, many still develop ibrutinib-resistant disease. Resistance can arise because mutations the ibrutinib-binding site BTK. Here, we characterized mechanism by which two mutations, C481F C481Y, may lead to resistance. Both mutants lacked detectable vitro...
DAO Diseases of Aquatic Organisms Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout JournalEditorsSpecials 38:67-70 (1999) - doi:10.3354/dao038067 Polymerase chain reaction (PCR) detection white spot syndrome virus (WSSV) in cultured and wild crustaceans India S. K. Otta, G. Shubha, B. Joseph, Anirban Chakraborty, Indrani Karunasagar, Iddya Karunasagar* Department Fishery Microbiology, University Agricultural Sciences,...
The ribosomal proteins (RPs) form the majority of cellular and are mandatory for growth. RP genes have been linked, either directly or indirectly, to various diseases in humans. Mutations also associated with tissue-specific phenotypes, suggesting a possible role organ development during early embryogenesis. However, it is not yet known how mutations particular gene result specific changes, might contribute human diseases. animal models defects will be essential studying these questions. In...
Summary Diamond–Blackfan anaemia (DBA) is a cancer‐prone genetic disorder characterized by pure red‐cell aplasia and associated physical deformities. The ribosomal protein S19 gene ( RPS19 ) the most frequently mutated in DBA (∼ 25%). TP53‐mediated cell cycle arrest and/or apoptosis erythroid cells have been suggested to be major factors for development, but it not clear why mutations ubiquitously expressed specifically affect erythropoiesis. Previously, we showed that deficiency zebrafish...
Eg5, a mitotic kinesin, has been target for anticancer drug development. Clinical trials of small-molecule inhibitors Eg5 have stymied by the development resistance, attributable to rescue different endogenous KIF15. Compared with relatively little is known about properties KIF15 motor. Here, we employed single-molecule optical-trapping techniques define mechanochemical cycle. We also studied inhibitory effects KIF15-IN-1, an uncharacterized, commercially available, inhibitor, on motility....
Colorectal cancer (CRC) is the third most prevalent cancer, while majority (80–85%) of CRCs are sporadic and microsatellite stable (MSS), approximately 15–20% them display instability (MSI). Infection chronic inflammation known to induce DNA damage in host tissues can lead oncogenic transformation cells, but role repair proteins microbe-associated remains unknown. Using CRC-associated microbes such as Fusobacterium nucleatum (Fn) a coculture with murine human enteroid-derived monolayers...
N -Glycidyl d -tryptophan ether derivative may be suitable for use as ointment base to reduce the inflammation, ROS, DNA damage and bacterial load over wounds.
Significance Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disease with no effective treatments. SCA3 etiologically linked to an abnormal polyglutamine (polyQ) tract at the C terminus of Ataxin-3 (ATXN3). How this polyQ stretch causes pathology remains elusive. Here we provide evidence that wild-type ATXN3 plays important role in error-free repair DNA double-strand breaks transcribed genes. In contrast, mutant blocks activity end-processing enzyme, polynucleotide kinase...
Abstract Mammalian polynucleotide kinase 3′-phosphatase (PNKP), a DNA end-processing enzyme with and 5′-kinase activities, is involved in multiple repair pathways, including base excision (BER), single-strand break (SSBR), double-strand (DSBR). However, little known as to how PNKP functions such diverse processes. Here we report that acetylated at K142 (AcK142) by p300 constitutively but K226 (AcK226) CBP, only after DSB induction. Co-immunoprecipitation analysis using AcK142 or AcK226...