Role of PatS and cell type on the heterocyst spacing pattern in a filamentous branching cyanobacterium

ABSTRACT Cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs) comprise major UV-induced photolesions. If left unrepaired, these lesions can induce mutations and skin cancer, which is facilitated by UV-induced immunosuppression. Yet the contribution of lesion and cell type specificity to the harmful biological effects of UV exposure remains currently unclear. Using a series of photolyase-transgenic mice to ubiquitously remove either CPDs or 6-4PPs from all cells in the mouse skin or selectively from basal keratinocytes, we show that the majority of UV-induced acute effects to require the presence of CPDs in basal keratinocytes in the mouse skin. At the fundamental level of gene expression, CPDs induce the expression of genes associated with repair and recombinational processing of DNA damage, as well as apoptosis and a response to stress. At the organismal level, photolyase-mediated removal of CPDs, but not 6-4PPs, from the genome of only basal keratinocytes substantially diminishes the incidence of skin tumors; however, it does not affect the UVB-mediated immunosuppression. Taken together, these findings reveal a differential role of basal keratinocytes in these processes, providing novel insights into the skin's acute and chronic responses to UV in a lesion- and cell-type-specific manner.

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THE ROLE OF THYMUS AND BONE MARROW CELLS IN DELAYED HYPERSENSITIVITY

Journal of Experimental Medicine ◽

10.1084/jem.134.5.1144 ◽

1971 ◽

Vol 134 (5) ◽

pp. 1144-1154 ◽

Cited By ~ 10

Author(s):

David G. Tubergen ◽

Joseph D. Feldman

Keyword(s):

Bone Marrow ◽

Bone Marrow Cells ◽

Specific Antigen ◽

Delayed Hypersensitivity ◽

Cell Type ◽

Skin Reactions ◽

Lymph Node Cells ◽

Thymus Cells ◽

Marrow Cells

Adoptive transfer experiments were performed to define the immunological role of thymus and bone marrow cells in the induction of delayed hypersensitivity (DH). The results indicated the following, (a) Bone marrow from immune donors contained cells capable of being stimulated by antigen to initiate the expression of DH. (b) Bone marrow from nonimmune or tolerant donors contained cells that were needed to complete the expression of DH after the infusion of immune lymph node cells. (c) Normal bone marrow and thymus cells cooperated in the irradiated recipient to induce the most vigorous skin reactions to specific antigen; these reactions were seen only when the recipients were stimulated by antigen. Either cell type alone was ineffective. (d) In the presence of tolerant bone marrow cells, thymus cells from immune donors gave a more vigorous response than did thymus cells from normal or tolerant donors. (e) There was suggestive evidence that thymus cells were the source of trigger elements that initiated DH. (f) Antigen in the irradiated recipient was necessary to induce DH after infusion of bone marrow cells alone, or bone marrow and thymus cells together.

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Blood viscosity during the neonatal period: The role of plasma and red blood cell type

The Journal of Pediatrics ◽

10.1016/s0022-3476(82)80458-7 ◽

1982 ◽

Vol 100 (3) ◽

pp. 449-453 ◽

Cited By ~ 12

Author(s):

Lise Riopel ◽

Jean-Claude Fouron ◽

Harry Bard

Keyword(s):

Blood Cell ◽

Red Blood Cell ◽

Blood Viscosity ◽

Neonatal Period ◽

Cell Type ◽

Blood Cell Type

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Autophagy-Lysosomal Pathway as Potential Therapeutic Target in Parkinson’s Disease

Cells ◽

10.3390/cells10123547 ◽

2021 ◽

Vol 10 (12) ◽

pp. 3547

Author(s):

Srinivasa Reddy Bonam ◽

Christine Tranchant ◽

Sylviane Muller

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Quality Control ◽

Cell Survival ◽

Control Systems ◽

Therapeutic Strategies ◽

Cell Type ◽

Potential Therapeutic Target ◽

Cellular Components

Cellular quality control systems have gained much attention in recent decades. Among these, autophagy is a natural self-preservation mechanism that continuously eliminates toxic cellular components and acts as an anti-ageing process. It is vital for cell survival and to preserve homeostasis. Several cell-type-dependent canonical or non-canonical autophagy pathways have been reported showing varying degrees of selectivity with regard to the substrates targeted. Here, we provide an updated review of the autophagy machinery and discuss the role of various forms of autophagy in neurodegenerative diseases, with a particular focus on Parkinson’s disease. We describe recent findings that have led to the proposal of therapeutic strategies targeting autophagy to alter the course of Parkinson’s disease progression.

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Faculty Opinions recommendation of Cell-Type-Specific Role of ΔFosB in Nucleus Accumbens In Modulating Intermale Aggression.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.733431968.793561598 ◽

2019 ◽

Author(s):

Klaus Miczek ◽

Herbert Covington III

Keyword(s):

Nucleus Accumbens ◽

Specific Role ◽

Cell Type ◽

Intermale Aggression ◽

Cell Type Specific

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IRE1-Mediated Unfolded Protein Response Promotes the Replication of Tick-Borne Flaviviruses in a Virus and Cell-Type Dependent Manner

Viruses ◽

10.3390/v13112164 ◽

2021 ◽

Vol 13 (11) ◽

pp. 2164

Author(s):

Veronika J. M. Breitkopf ◽

Gerhard Dobler ◽

Peter Claus ◽

Hassan Y. Naim ◽

Imke Steffen

Keyword(s):

Unfolded Protein Response ◽

Intestinal Cell ◽

Intestinal Cells ◽

Tissue Tropism ◽

Cell Type ◽

Unfolded Protein ◽

Tbev Strain ◽

The Unfolded Protein Response ◽

Protein Response

Tick-borne flaviviruses (TBFV) can cause severe neurological complications in humans, but differences in tissue tropism and pathogenicity have been described for individual virus strains. Viral protein synthesis leads to the induction of the unfolded protein response (UPR) within infected cells. The IRE1 pathway has been hypothesized to support flavivirus replication by increasing protein and lipid biogenesis. Here, we investigated the role of the UPR in TBFV infection in human astrocytes, neuronal and intestinal cell lines that had been infected with tick-borne encephalitis virus (TBEV) strains Neudoerfl and MucAr-HB-171/11 as well as Langat virus (LGTV). Both TBEV strains replicated better than LGTV in central nervous system (CNS) cells. TBEV strain MucAr-HB-171/11, which is associated with gastrointestinal symptoms, replicated best in intestinal cells. All three viruses activated the inositol-requiring enzyme 1 (IRE1) pathway via the X-box binding protein 1 (XBP1). Interestingly, the neurotropic TBEV strain Neudoerfl induced a strong upregulation of XBP1 in all cell types, but with faster kinetics in CNS cells. In contrast, TBEV strain MucAr-HB-171/11 failed to activate the IRE1 pathway in astrocytes. The low pathogenic LGTV led to a mild induction of IRE1 signaling in astrocytes and intestinal cells. When cells were treated with IRE1 inhibitors prior to infection, TBFV replication in astrocytes was significantly reduced. This confirms a supporting role of the IRE1 pathway for TBFV infection in relevant viral target cells and suggests a correlation between viral tissue tropism and the cell-type dependent induction of the unfolded protein response.

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The role of scale in the estimation of cell-type proportions

The Annals of Applied Statistics ◽

10.1214/20-aoas1395 ◽

2021 ◽

Vol 15 (1) ◽

Author(s):

Gregory J. Hunt ◽

Johann A. Gagnon-Bartsch

Keyword(s):

Cell Type

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Autophagy in endocrine tumors

Endocrine Related Cancer ◽

10.1530/erc-15-0042 ◽

2015 ◽

Vol 22 (4) ◽

pp. R205-R218 ◽

Cited By ~ 20

Author(s):

Andrea Weckman ◽

Fabio Rotondo ◽

Antonio Di Ieva ◽

Luis V Syro ◽

Henriett Butz ◽

...

Keyword(s):

Treatment Efficacy ◽

Endocrine Tumors ◽

Dependent Manner ◽

Endocrine Glands ◽

Cell Type ◽

Pathological Conditions ◽

Tumor Survival ◽

Different Types ◽

Intracellular Process

Autophagy is an important intracellular process involving the degradation of cytoplasmic components. It is involved in both physiological and pathological conditions, including cancer. The role of autophagy in cancer is described as a ‘double-edged sword,’ a term that reflects its known participation in tumor suppression, tumor survival and tumor cell proliferation. Available research regarding autophagy in endocrine cancer supports this concept. Autophagy shows promise as a novel therapeutic target in different types of endocrine cancer, inhibiting or increasing treatment efficacy in a context- and cell-type-dependent manner. At present, however, there is very little research concerning autophagy in endocrine tumors. No research was reported connecting autophagy to some of the tumors of the endocrine glands such as the pancreas and ovary. This review aims to elucidate the roles of autophagy in different types of endocrine cancer and highlight the need for increased research in the field.

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Target-specific M1 inputs to infragranular S1 pyramidal neurons

Journal of Neurophysiology ◽

10.1152/jn.01032.2015 ◽

2016 ◽

Vol 116 (3) ◽

pp. 1261-1274 ◽

Cited By ~ 11

Author(s):

Amanda K. Kinnischtzke ◽

Erika E. Fanselow ◽

Daniel J. Simons

Keyword(s):

Primary Motor Cortex ◽

Pyramidal Neurons ◽

Projection Neurons ◽

Cell Type ◽

Intrinsic Properties ◽

Subcortical Structures ◽

Medial Nucleus ◽

Cell Type Specific ◽

Posterior Medial Nucleus

The functional role of input from the primary motor cortex (M1) to primary somatosensory cortex (S1) is unclear; one key to understanding this pathway may lie in elucidating the cell-type specific microcircuits that connect S1 and M1. Recently, we discovered that a subset of pyramidal neurons in the infragranular layers of S1 receive especially strong input from M1 (Kinnischtzke AK, Simons DJ, Fanselow EE. Cereb Cortex 24: 2237–2248, 2014), suggesting that M1 may affect specific classes of pyramidal neurons differently. Here, using combined optogenetic and retrograde labeling approaches in the mouse, we examined the strengths of M1 inputs to five classes of infragranular S1 neurons categorized by their projections to particular cortical and subcortical targets. We found that the magnitude of M1 synaptic input to S1 pyramidal neurons varies greatly depending on the projection target of the postsynaptic neuron. Of the populations examined, M1-projecting corticocortical neurons in L6 received the strongest M1 inputs, whereas ventral posterior medial nucleus-projecting corticothalamic neurons, also located in L6, received the weakest. Each population also possessed distinct intrinsic properties. The results suggest that M1 differentially engages specific classes of S1 projection neurons, thereby regulating the motor-related influence S1 exerts over subcortical structures.

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