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Modulation of T Cell Cytokine Production by Interferon Regulatory Factor-4*
Stable expression of IRF-4 in Jurkat T cells not only leads to a strong enhancement in the synthesis of interleukin (IL)-2, but also enables these cells to start producing considerable amounts of IL-4, IL-10, and IL-13. Expand
Loss of IRF-4-binding protein leads to the spontaneous development of systemic autoimmunity.
It is demonstrated that loss of IBP leads to the spontaneous development of a systemic autoimmune disorder characterized by the accumulation of effector/memory T cells and IgG+ B cells, profound hypergammaglobulinemia, and autoantibody production. Expand
T Cell Receptor Engagement Leads to the Recruitment of IBP, a Novel Guanine Nucleotide Exchange Factor, to the Immunological Synapse*
Findings indicate that other GEFs, such as IBP, also relocalize to this intercellular region, and the recruitment and activation of distinct classes of GEFs may allow for precise control of Rho GTPase function at the crucial interface between T cells and antigen presenting cells. Expand
Actin Polymerization Is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration
It is found that new filamentous actin polymerization occurs in the SLI of mouse sciatic nerves after injury and that its inhibition prevented not only the degradation of E-cadherin in the SLI but also myelin ovoid formation. Expand
Autophagic myelin destruction by schwann cells during wallerian degeneration and segmental demyelination
The findings suggest that autophagy is the self‐myelin destruction mechanism of Schwann cells, but mechanistically, it is a process distinct from Schwann cell plasticity for nerve repair. Expand
Autophagy Is Involved in the Reduction of Myelinating Schwann Cell Cytoplasm during Myelin Maturation of the Peripheral Nerve
Peripheral nerve myelination involves dynamic changes in Schwann cell morphology and membrane structure. Recent studies have demonstrated that autophagy regulates organelle biogenesis and plasmaExpand
Suppression of beta-N-acetylglucosaminidase in the N-glycosylation pathway for complex glycoprotein formation in Drosophila S2 cells.
The data demonstrate that GlcNAcase may be an important factor in the formation of paucimannosidic core N-glycans in Drosophila S2 cells and suggest that it may be possible to express complex glycoproteins in engineered Drosophile S1 cells by suppressing Glc NAcase in the N- glycosylation pathway. Expand
Pathological adaptive responses of Schwann cells to endoplasmic reticulum stress in bortezomib‐induced peripheral neuropathy
The findings in this study suggest that the pathological adaptive responses of Schwann cells to bortezomib‐induced ER stress may, in part, participate in the development of BIPN. Expand
Expression of β-1,4-galactosyltransferase and suppression of β-N-acetylglucosaminidase to aid synthesis of complex N-glycans in insect Drosophila S2 cells.
It will be possible to express a complete functional human glycoprotein in engineered Drosophila S2 cells by suppressing GlcNAcase and co-expressing additional glycosyltransferases of N-glycosylation pathway, according to the present work. Expand
The Neuregulin‐Rac‐MKK7 pathway regulates antagonistic c‐jun/Krox20 expression in Schwann cell dedifferentiation
It is demonstrated that active Rac1 GTPase functions as a negative regulator of Schwann cell differentiation by upregulating c‐jun and downregulating Krox20 through the MKK7‐JNK pathway, but not through the Raf‐ERK pathway. Expand