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  • 1
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    Spatiotemporal dynamics of molecular pathology in amyotrophic lateral sclerosis (2019)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2019
    Description: 〈p〉Paralysis occurring in amyotrophic lateral sclerosis (ALS) results from denervation of skeletal muscle as a consequence of motor neuron degeneration. Interactions between motor neurons and glia contribute to motor neuron loss, but the spatiotemporal ordering of molecular events that drive these processes in intact spinal tissue remains poorly understood. Here, we use spatial transcriptomics to obtain gene expression measurements of mouse spinal cords over the course of disease, as well as of postmortem tissue from ALS patients, to characterize the underlying molecular mechanisms in ALS. We identify pathway dynamics, distinguish regional differences between microglia and astrocyte populations at early time points, and discern perturbations in several transcriptional pathways shared between murine models of ALS and human postmortem spinal cords.〈/p〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Constitutive display of cryptic translation products by MHC class I molecules (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Major histocompatibility complex (MHC) class I molecules display tens of thousands of peptides on the cell surface, derived from virtually all endogenous proteins, for inspection by cytotoxic T cells (CTLs). We show that, in normal mouse cells, MHC I molecules present a peptide encoded in the 3' "untranslated" region. Despite its rarity, the peptide elicits CTL responses and induces self-tolerance, establishing that immune surveillance extends well beyond conventional polypeptides. Furthermore, translation of this cryptic peptide occurs by a previously unknown mechanism that decodes the CUG initiation codon as leucine rather than the canonical methionine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwab, Susan R -- Li, Katy C -- Kang, Chulho -- Shastri, Nilabh -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1367-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958358" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Amino Acid Sequence ; Animals ; *Antigen Presentation ; B-Lymphocytes/metabolism ; Base Sequence ; Codon, Initiator ; Codon, Terminator ; Dendritic Cells/immunology/metabolism ; Female ; Fibroblasts/metabolism ; H-2 Antigens/*immunology ; Hybridomas ; Leucine/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Minor Histocompatibility Antigens/genetics ; Molecular Sequence Data ; Peptides/*genetics/*immunology ; *Protein Biosynthesis ; Proteins/genetics ; Self Tolerance ; Spleen/cytology/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Crystal structure of the T4 regA translational regulator protein at 1.9 A resolution (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-26
    Description: The translational regulator protein regA is encoded by the T4 bacteriophage and binds to a region of messenger RNA (mRNA) that includes the initiator codon. RegA is unusual in that it represses the translation of about 35 early T4 mRNAs but does not affect nearly 200 other mRNAs. The crystal structure of regA was determined at 1.9 A resolution; the protein was shown to have an alpha-helical core and two regions with antiparallel beta sheets. One of these beta sheets has four antiparallel strands and has some sequence homology to RNP-1 and RNP-2, which are believed to be RNA-binding motifs and are found in a number of known RNA-binding proteins. Structurally guided mutants may help to uncover the basis for this variety of RNA interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, C -- Chan, R -- Berger, I -- Lockshin, C -- Green, L -- Gold, L -- Rich, A -- New York, N.Y. -- Science. 1995 May 26;268(5214):1170-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761833" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacteriophage T4/*chemistry ; Crystallography, X-Ray ; Models, Molecular ; Molecular Sequence Data ; Protein Structure, Secondary ; RNA-Binding Proteins/*chemistry ; Structure-Activity Relationship ; Viral Proteins/*chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Recognition of a ubiquitous self antigen by prostate cancer-infiltrating CD8+ T lymphocytes (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-12
    Description: Substantial evidence exists that many tumors can be specifically recognized by CD8+ T lymphocytes. The definition of antigens targeted by these cells is paramount for the development of effective immunotherapeutic strategies for treating human cancers. In a screen for endogenous tumor-associated T cell responses in a primary mouse model of prostatic adenocarcinoma, we identified a naturally arising CD8+ T cell response that is reactive to a peptide derived from histone H4. Despite the ubiquitous nature of histones, T cell recognition of histone H4 peptide was specifically associated with the presence of prostate cancer in these mice. Thus, the repertoire of antigens recognized by tumor-infiltrating T cells is broader than previously thought and includes peptides derived from ubiquitous self antigens that are normally sequestered from immune detection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savage, Peter A -- Vosseller, Keith -- Kang, Chulho -- Larimore, Kevin -- Riedel, Elyn -- Wojnoonski, Kathleen -- Jungbluth, Achim A -- Allison, James P -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):215-20. doi: 10.1126/science.1148886.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Howard Hughes Medical Institute, and Ludwig Center for Cancer Immunotherapy, Memorial Sloan-Kettering Cancer Center (MSKCC), New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187659" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*immunology ; Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens, Neoplasm/*immunology ; Autoantigens/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Line ; Epitopes, T-Lymphocyte/immunology ; Histones/*immunology ; Hybridomas ; Lymphocytes, Tumor-Infiltrating/*immunology ; Male ; Mice ; Mice, Transgenic ; Peptide Fragments/immunology ; Prostatic Neoplasms/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    FBXW7 targets mTOR for degradation and cooperates with PTEN in tumor suppression (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-13
    Description: The enzyme mTOR (mammalian target of rapamycin) is a major target for therapeutic intervention to treat many human diseases, including cancer, but very little is known about the processes that control levels of mTOR protein. Here, we show that mTOR is targeted for ubiquitination and consequent degradation by binding to the tumor suppressor protein FBXW7. Human breast cancer cell lines and primary tumors showed a reciprocal relation between loss of FBXW7 and deletion or mutation of PTEN (phosphatase and tensin homolog), which also activates mTOR. Tumor cell lines harboring deletions or mutations in FBXW7 are particularly sensitive to rapamycin treatment, which suggests that loss of FBXW7 may be a biomarker for human cancers susceptible to treatment with inhibitors of the mTOR pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849753/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849753/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Jian-Hua -- Kim, Il-Jin -- Wu, Di -- Climent, Joan -- Kang, Hio Chung -- DelRosario, Reyno -- Balmain, Allan -- R01 CA116481/CA/NCI NIH HHS/ -- U01 CA084244/CA/NCI NIH HHS/ -- U01 CA084244-08/CA/NCI NIH HHS/ -- U01 CA084244-09/CA/NCI NIH HHS/ -- U01 CA084244-10/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1499-502. doi: 10.1126/science.1162981.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Institute, University of California at San Francisco, 2340 Sutter Street, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/drug therapy/genetics/*metabolism/pathology ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; F-Box Proteins/genetics/*metabolism ; Gene Deletion ; Gene Dosage ; Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Nude ; Mutation ; Neoplasm Transplantation ; PTEN Phosphohydrolase/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/pharmacology/therapeutic use ; TOR Serine-Threonine Kinases ; Transfection ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Nonlegumes respond to rhizobial Nod factors by suppressing the innate immune response (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-07
    Description: Virtually since the discovery of nitrogen-fixing Rhizobium-legume symbioses, researchers have dreamed of transferring this capability into nonlegume crop species (for example, corn). In general, nonlegumes were assumed to lack the ability to respond to the rhizobial lipo-chitin Nod factors, which are the essential signal molecules that trigger legume nodulation. However, our data indicate that Arabidopsis thaliana plants, as well as other nonlegumes, recognize the rhizobial Nod factor via a mechanism that results in strong suppression of microbe-associated molecular pattern (MAMP)-triggered immunity. The mechanism of action leads to reduced levels of pattern-recognition receptors on the plasma membrane involved in MAMP recognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liang, Yan -- Cao, Yangrong -- Tanaka, Kiwamu -- Thibivilliers, Sandra -- Wan, Jinrong -- Choi, Jeongmin -- Kang, Chang ho -- Qiu, Jing -- Stacey, Gary -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1384-7. doi: 10.1126/science.1242736. Epub 2013 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Plant Science, National Center for Soybean Biotechnology, Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009356" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/drug effects/*immunology/*microbiology ; Arabidopsis Proteins/metabolism ; Cell Membrane/metabolism ; Flagellin/immunology ; Immunity, Innate/drug effects/*immunology ; Lipopolysaccharides/*immunology/pharmacology ; Nitrogen Fixation/genetics ; Oligosaccharides/immunology/pharmacology ; Protein Kinases/metabolism ; Proteolysis ; Receptors, Pattern Recognition/metabolism ; Soybeans/immunology/microbiology ; Symbiosis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Aire-dependent thymic development of tumor-associated regulatory T cells (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-09
    Description: Despite considerable interest in the modulation of tumor-associated Foxp3(+) regulatory T cells (T(regs)) for therapeutic benefit, little is known about the developmental origins of these cells and the nature of the antigens that they recognize. We identified an endogenous population of antigen-specific T(regs) (termed MJ23 T(regs)) found recurrently enriched in the tumors of mice with oncogene-driven prostate cancer. MJ23 T(regs) were not reactive to a tumor-specific antigen but instead recognized a prostate-associated antigen that was present in tumor-free mice. MJ23 T(regs) underwent autoimmune regulator (Aire)-dependent thymic development in both male and female mice. Thus, Aire-mediated expression of peripheral tissue antigens drives the thymic development of a subset of organ-specific T(regs), which are likely coopted by tumors developing within the associated organ.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3622085/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3622085/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malchow, Sven -- Leventhal, Daniel S -- Nishi, Saki -- Fischer, Benjamin I -- Shen, Lynn -- Paner, Gladell P -- Amit, Ayelet S -- Kang, Chulho -- Geddes, Jenna E -- Allison, James P -- Socci, Nicholas D -- Savage, Peter A -- 1R01CA160371-01/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30 CA14599/CA/NCI NIH HHS/ -- R01 CA160371/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Mar 8;339(6124):1219-24. doi: 10.1126/science.1233913.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23471412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, Polyomavirus Transforming/genetics ; Autoantigens/immunology ; Female ; Forkhead Transcription Factors/analysis ; Homeodomain Proteins/genetics ; *Immune Tolerance ; Male ; Mice ; Mice, Transgenic ; Prostate/*immunology ; Prostate-Specific Antigen/immunology ; Prostatic Neoplasms/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Thymus Gland/*growth & development/*immunology ; Transcription Factors/genetics/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-26
    Description: Cellular senescence is a terminal stress-activated program controlled by the p53 and p16(INK4a) tumor suppressor proteins. A striking feature of senescence is the senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promotion and aging. We have identified the transcription factor GATA4 as a senescence and SASP regulator. GATA4 is stabilized in cells undergoing senescence and is required for the SASP. Normally, GATA4 is degraded by p62-mediated selective autophagy, but this regulation is suppressed during senescence, thereby stabilizing GATA4. GATA4 in turn activates the transcription factor NF-kappaB to initiate the SASP and facilitate senescence. GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a). GATA4 accumulates in multiple tissues, including the aging brain, and could contribute to aging and its associated inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Chanhee -- Xu, Qikai -- Martin, Timothy D -- Li, Mamie Z -- Demaria, Marco -- Aron, Liviu -- Lu, Tao -- Yankner, Bruce A -- Campisi, Judith -- Elledge, Stephen J -- AG009909/AG/NIA NIH HHS/ -- AG017242/AG/NIA NIH HHS/ -- AG046174/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):aaa5612. doi: 10.1126/science.aaa5612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Buck Institute for Research on Aging, Novato, CA 94945, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. selledge@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404840" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Autophagy/*genetics ; Brain/metabolism ; Cell Aging/*genetics ; Cell Cycle/genetics ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16 ; *DNA Damage ; Fibroblasts ; GATA4 Transcription Factor/genetics/*metabolism ; Gene Expression Profiling ; Humans ; Inflammation/*genetics ; Interleukin-1alpha/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/metabolism ; NF-kappa B/metabolism ; Phenotype ; Promoter Regions, Genetic ; Tumor Necrosis Factor Receptor-Associated Peptides and ; Proteins/genetics/metabolism ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Stretchable self-healable semiconducting polymer film for active-matrix strain-sensing array (2019)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2019
    Description: 〈p〉Skin-like sensory devices should be stretchable and self-healable to meet the demands for future electronic skin applications. Despite recent notable advances in skin-inspired electronic materials, it remains challenging to confer these desired functionalities to an active semiconductor. Here, we report a strain-sensitive, stretchable, and autonomously self-healable semiconducting film achieved through blending of a polymer semiconductor and a self-healable elastomer, both of which are dynamically cross-linked by metal coordination. We observed that by controlling the percolation threshold of the polymer semiconductor, the blend film became strain sensitive, with a gauge factor of 5.75 x 10〈sup〉5〈/sup〉 at 100% strain in a stretchable transistor. The blend film is also highly stretchable (fracture strain, 〉1300%) and autonomously self-healable at room temperature. We proceed to demonstrate a fully integrated 5 x 5 stretchable active-matrix transistor sensor array capable of detecting strain distribution through surface deformation.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Structural basis for KCNE3 modulation of potassium recycling in epithelia (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-09-11
    Description: The single-span membrane protein KCNE3 modulates a variety of voltage-gated ion channels in diverse biological contexts. In epithelial cells, KCNE3 regulates the function of the KCNQ1 potassium ion (K + ) channel to enable K + recycling coupled to transepithelial chloride ion (Cl – ) secretion, a physiologically critical cellular transport process in various organs and whose malfunction causes diseases, such as cystic fibrosis (CF), cholera, and pulmonary edema. Structural, computational, biochemical, and electrophysiological studies lead to an atomically explicit integrative structural model of the KCNE3-KCNQ1 complex that explains how KCNE3 induces the constitutive activation of KCNQ1 channel activity, a crucial component in K + recycling. Central to this mechanism are direct interactions of KCNE3 residues at both ends of its transmembrane domain with residues on the intra- and extracellular ends of the KCNQ1 voltage-sensing domain S4 helix. These interactions appear to stabilize the activated "up" state configuration of S4, a prerequisite for full opening of the KCNQ1 channel gate. In addition, the integrative structural model was used to guide electrophysiological studies that illuminate the molecular basis for how estrogen exacerbates CF lung disease in female patients, a phenomenon known as the "CF gender gap."
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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