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  1. Article ; Online: TCR microclusters form spatially segregated domains and sequentially assemble in calcium-dependent kinetic steps

    Jason Yi / Lakshmi Balagopalan / Tiffany Nguyen / Katherine M. McIntire / Lawrence E. Samelson

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 13

    Abstract: Engagement of T cell receptors (TCRs) induces the formation of microclusters that mediate the downstream signalling events. Here the authors show, using high resolution TIRF-SIM and live cell imaging, that ZAP70 and LAT are recruited to TCR with distinct ...

    Abstract Engagement of T cell receptors (TCRs) induces the formation of microclusters that mediate the downstream signalling events. Here the authors show, using high resolution TIRF-SIM and live cell imaging, that ZAP70 and LAT are recruited to TCR with distinct kinetics, with the delayed ZAP70-TCR association modulated by TCR-induced calcium flux.
    Keywords Science ; Q
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: TCR microclusters form spatially segregated domains and sequentially assemble in calcium-dependent kinetic steps

    Jason Yi / Lakshmi Balagopalan / Tiffany Nguyen / Katherine M. McIntire / Lawrence E. Samelson

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 13

    Abstract: Engagement of T cell receptors (TCRs) induces the formation of microclusters that mediate the downstream signalling events. Here the authors show, using high resolution TIRF-SIM and live cell imaging, that ZAP70 and LAT are recruited to TCR with distinct ...

    Abstract Engagement of T cell receptors (TCRs) induces the formation of microclusters that mediate the downstream signalling events. Here the authors show, using high resolution TIRF-SIM and live cell imaging, that ZAP70 and LAT are recruited to TCR with distinct kinetics, with the delayed ZAP70-TCR association modulated by TCR-induced calcium flux.
    Keywords Science ; Q
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  3. Article ; Online: Bypassing ubiquitination enables LAT recycling to the cell surface and enhanced signaling in T cells.

    Lakshmi Balagopalan / Hiba Malik / Katherine M McIntire / Joseph A Garvey / Tiffany Nguyen / Ana B Rodriguez-Peña / Lawrence E Samelson

    PLoS ONE, Vol 15, Iss 2, p e

    2020  Volume 0229036

    Abstract: LAT molecules defective in ubiquitination have an increased half-life and induce enhanced signaling when expressed in T cells. In this study, we have examined the role of ubiquitination in regulating LAT endocytosis, recycling, and degradation in resting ...

    Abstract LAT molecules defective in ubiquitination have an increased half-life and induce enhanced signaling when expressed in T cells. In this study, we have examined the role of ubiquitination in regulating LAT endocytosis, recycling, and degradation in resting and stimulated T cells. By tracking and comparing plasma membrane-labeled wild type and ubiquitination-resistant 2KR LAT, we find that ubiquitination promotes the degradation of surface LAT in T cells. Activation of T cells increases LAT ubiquitination and promotes trafficking of internalized LAT to lysosomes for degradation. Ubiquitination of LAT does not change internalization rates from the cell surface, but prevents efficient recycling of LAT to the surface of T cells. Our study demonstrates that surface LAT levels are tightly controlled by ubiquitination. LAT in unstimulated cells lacks ubiquitin allowing for increased LAT stability and efficient T cell activation upon TCR triggering; ubiquitination leads to efficient removal of LAT after activation.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Functional analysis of SLC39A8 mutations and their implications for manganese deficiency and mitochondrial disorders

    Eun-Kyung Choi / Trang-Tiffany Nguyen / Neil Gupta / Shigeki Iwase / Young Ah Seo

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Volume 17

    Abstract: Abstract SLC39A8 encodes ZIP8, a divalent metal ion transporter. Mutations in the SLC39A8 gene are associated with congenital disorder of glycosylation type II and Leigh syndrome. Notably, affected patients with both disorders exhibited severe manganese ( ...

    Abstract Abstract SLC39A8 encodes ZIP8, a divalent metal ion transporter. Mutations in the SLC39A8 gene are associated with congenital disorder of glycosylation type II and Leigh syndrome. Notably, affected patients with both disorders exhibited severe manganese (Mn) deficiency. The cellular function of human SLC39A8 (hSLC39A8) and the mechanisms by which mutations in this protein lead to human diseases are unclear. Herein, we show that hSLC39A8 mediates 54Mn uptake by the cells, and its expression is regulated by Mn. While expression of wild-type hSLC39A8 increased 54Mn uptake activity, disease-associated mutations abrogated the ability of the transporter to mediate Mn uptake into the cells, thereby providing a causal link to severe Mn deficiency. All mutants failed to localize on the cell surface and were retained within the endoplasmic reticulum. Interestingly, expression of hSLC39A8 mutants of both CDG type II and Leigh syndrome reduced mitochondrial 54Mn levels and activity of Mn-dependent mitochondrial superoxide dismutase MnSOD, and in turn increased oxidative stress. The expression of wild-type hSLC39A8, but not the disease-associated mutants, promoted mitochondrial functions. Moreover, loss of function analyses further corroborate hSLC39A8’s critical role in mediating Mn uptake and mitochondrial function. Our results provide a potential pathogenic mechanism of diseases that are associated with hSLC39A8 mutations.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570 ; 610
    Language English
    Publishing date 2018-02-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Plasma membrane LAT activation precedes vesicular recruitment defining two phases of early T-cell activation

    Lakshmi Balagopalan / Jason Yi / Tiffany Nguyen / Katherine M. McIntire / Adam S. Harned / Kedar Narayan / Lawrence E. Samelson

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 17

    Abstract: Controversy exists over the function of plasma membrane versus intracellular vesicular LAT in T-cell receptor signaling. Here the authors use high resolution imaging of the temporal dynamics of LAT involvement to show that both sources of LAT are ... ...

    Abstract Controversy exists over the function of plasma membrane versus intracellular vesicular LAT in T-cell receptor signaling. Here the authors use high resolution imaging of the temporal dynamics of LAT involvement to show that both sources of LAT are required, but at distinct stages.
    Keywords Science ; Q
    Language English
    Publishing date 2018-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  6. Article ; Online: Intracerebral Delivery of Brain-Derived Neurotrophic Factor Using HyStem ® -C Hydrogel Implants Improves Functional Recovery and Reduces Neuroinflammation in a Rat Model of Ischemic Stroke

    Kristine Ravina / Denise I. Briggs / Sezen Kislal / Zuha Warraich / Tiffany Nguyen / Rachel K. Lam / Thomas I. Zarembinski / Mehrdad Shamloo

    International Journal of Molecular Sciences, Vol 19, Iss 12, p

    2018  Volume 3782

    Abstract: Ischemic stroke is a leading cause of death and disability worldwide. Potential therapeutics aimed at neural repair and functional recovery are limited in their blood-brain barrier permeability and may exert systemic or off-target effects. We examined ... ...

    Abstract Ischemic stroke is a leading cause of death and disability worldwide. Potential therapeutics aimed at neural repair and functional recovery are limited in their blood-brain barrier permeability and may exert systemic or off-target effects. We examined the effects of brain-derived neurotrophic factor (BDNF), delivered via an extended release HyStem ® -C hydrogel implant or vehicle, on sensorimotor function, infarct volume, and neuroinflammation, following permanent distal middle cerebral artery occlusion (dMCAo) in rats. Eight days following dMCAo or sham surgery, treatments were implanted directly into the infarction site. Rats received either vehicle, BDNF-only (0.167 µg/µL), hydrogel-only, hydrogel impregnated with 0.057 µg/µL of BDNF (hydrogel + BDNF LOW ), or hydrogel impregnated with 0.167 µg/µL of BDNF (hydrogel + BDNF HIGH ). The adhesive removal test (ART) and 28-point Neuroscore (28-PN) were used to evaluate sensorimotor function up to two months post-ischemia. The hydrogel + BDNF HIGH group showed significant improvements on the ART six to eight weeks following treatment and their behavioral performance was consistently greater on the 28-PN. Infarct volume was reduced in rats treated with hydrogel + BDNF HIGH as were levels of microglial, phagocyte, and astrocyte marker immunoexpression in the corpus striatum. These data suggest that targeted intracerebral delivery of BDNF using hydrogels may mitigate ischemic brain injury and restore functional deficits by reducing neuroinflammation.
    Keywords brain-derived neurotrophic factor ; functional recovery ; hydrogel ; ischemic stroke ; neuroinflammation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 616
    Language English
    Publishing date 2018-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  7. Article ; Online: Lipid peroxidation regulates podocyte migration and cytoskeletal structure through redox sensitive RhoA signaling

    Claudia Kruger / Susan J. Burke / J. Jason Collier / Trang-Tiffany Nguyen / J. Michael Salbaum / Krisztian Stadler

    Redox Biology, Vol 16, Iss , Pp 248-

    2018  Volume 254

    Abstract: Early podocyte loss is characteristic of chronic kidney diseases (CKD) in obesity and diabetes. Since treatments for hyperglycemia and hypertension do not prevent podocyte loss, there must be additional factors causing podocyte depletion. The role of ... ...

    Abstract Early podocyte loss is characteristic of chronic kidney diseases (CKD) in obesity and diabetes. Since treatments for hyperglycemia and hypertension do not prevent podocyte loss, there must be additional factors causing podocyte depletion. The role of oxidative stress has been implicated in CKD but it is not known how exactly free radicals affect podocyte physiology. To assess this relationship, we investigated the effects of lipid radicals on podocytes, as lipid peroxidation is a major form of oxidative stress in diabetes. We found that lipid radicals govern changes in podocyte homeostasis through redox sensitive RhoA signaling: lipid radicals inhibit migration and cause loss of F-actin fibers. These effects were prevented by mutating the redox sensitive cysteines of RhoA. We therefore suggest that in diseases associated with increased lipid peroxidation, lipid radicals can determine podocyte function with potentially pathogenic consequences for kidney physiology. Keywords: Lipid peroxidation, Reactive lipids, Podocyte, RhoA, Cysteine, Chronic kidney disease
    Keywords Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Subject code 500
    Language English
    Publishing date 2018-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Plasma membrane LAT activation precedes vesicular recruitment defining two phases of early T-cell activation

    Lakshmi Balagopalan / Jason Yi / Tiffany Nguyen / Katherine M. McIntire / Adam S. Harned / Kedar Narayan / Lawrence E. Samelson

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 17

    Abstract: Controversy exists over the function of plasma membrane versus intracellular vesicular LAT in T-cell receptor signaling. Here the authors use high resolution imaging of the temporal dynamics of LAT involvement to show that both sources of LAT are ... ...

    Abstract Controversy exists over the function of plasma membrane versus intracellular vesicular LAT in T-cell receptor signaling. Here the authors use high resolution imaging of the temporal dynamics of LAT involvement to show that both sources of LAT are required, but at distinct stages.
    Keywords Science ; Q
    Language English
    Publishing date 2018-05-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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