scholarly journals Impaired epidermal Langerhans cell maturation in TGFβ-inducible early gene 1 (TIEG1) knockout mice

Oncotarget ◽  
2017 ◽  
Vol 8 (68) ◽  
pp. 112875-112882 ◽  
Author(s):  
Xilin Zhang ◽  
Yi Yao ◽  
Wei-Zen Wei ◽  
Zeng-Quan Yang ◽  
Jun Gu ◽  
...  
2006 ◽  
Vol 105 (1) ◽  
pp. 48-54 ◽  
Author(s):  
T NOJIMA ◽  
K HAYASHI ◽  
R GOITSUKA ◽  
K NAKAYAMA ◽  
K NAKAYAMA ◽  
...  

2008 ◽  
Vol 11 (02) ◽  
pp. 63-69 ◽  
Author(s):  
Manabu Taguchi ◽  
Steven L. Moran ◽  
Mark E. Zobitz ◽  
Chunfeng Zhao ◽  
Malayannan Subramaniam ◽  
...  

Transforming growth factor beta (TGF-β) has a broad effect on wound healing, but many questions remain about the regulation of TGF-β during the healing process. TGF-β inducible early gene 1 (TIEG1) is a primary response gene for TGF-β that controls the activities of the TGF-β/Smad pathway, the primary TGF-β signaling pathway. The purpose of this study was to investigate the role of TIEG1 in cutaneous wound healing using TIEG1 knockout mice. The wound healing in TIEG1 knockout mice and wild-type controls was evaluated by wound breaking strength, Western blot, and histology at postoperative days 3, 7, and 14. Although re-epithelialization of both groups was similarly complete at day 7, the TIEG1 knockout mice had a significantly lower wound breaking strength than the controls at postoperative day 14. These results suggest that TIEG1 expression may be an important factor involved in the initiation and support of normal cutaneous wound healing.


2012 ◽  
Vol 16 (2) ◽  
pp. 405-415 ◽  
Author(s):  
Madhurima Benekareddy ◽  
Amrita R. Nair ◽  
Brian G. Dias ◽  
Deepika Suri ◽  
Anita E. Autry ◽  
...  

Abstract Exposure to stress and hallucinogens in adulthood evokes persistent alterations in neurocircuitry and emotional behaviour. The structural and functional changes induced by stress and hallucinogen exposure are thought to involve transcriptional alterations in specific effector immediate early genes. The immediate early gene, activity regulated cytoskeletal-associated protein (Arc), is important for both activity and experience dependent plasticity. We sought to examine whether trophic factor signalling through brain-derived neurotrophic factor (BDNF) contributes to the neocortical regulation of Arc mRNA in response to distinct stimuli such as immobilization stress and the hallucinogen 2,5-dimethoxy-4-iodoamphetamine (DOI). Acute exposure to either immobilization stress or DOI induced Arc mRNA levels within the neocortex. BDNF infusion into the neocortex led to a robust up-regulation of local Arc transcript expression. Further, baseline Arc mRNA expression in the neocortex was significantly decreased in inducible BDNF knockout mice with an adult-onset, forebrain specific BDNF loss. The induction of Arc mRNA levels in response to both acute immobilization stress or a single administration of DOI was significantly attenuated in the inducible BDNF knockout mice. Taken together, our results implicate trophic factor signalling through BDNF in the regulation of cortical Arc mRNA expression, both under baseline conditions and following stress and hallucinogen exposure. These findings suggest the possibility that the regulation of Arc expression via BDNF provides a molecular substrate for the structural and synaptic plasticity observed following stimuli such as stress and hallucinogens.


2021 ◽  
Author(s):  
Zewen K. Tuong ◽  
Samuel W. Lukowski ◽  
Quan H. Nguyen ◽  
Janin Chandra ◽  
Chenhao Zhou ◽  
...  

1996 ◽  
Vol 184 (4) ◽  
pp. 1537-1541 ◽  
Author(s):  
C M Snapper ◽  
F R Rosas ◽  
P Zelazowski ◽  
M A Moorman ◽  
M R Kehry ◽  
...  

A number of distinct functional abnormalities have been observed in B cells derived from p50/ NF-kappa B or c-rel knockout mice. RelB, another member of the NF-kappa B/Rel family of transcription factors, is expressed during the latter stages of B cell maturation and can bind to regulatory sites within the Ig heavy chain locus. Therefore, we tested the ability of B cells from relB knockout mice (relB-/-) to proliferate, undergo maturation to IgM secretion, and switch to the expression of downstream Ig isotypes in response to distinct activators including LPS, anti-CD40 mAb or CD40 ligand, and/or dextran anti-IgD antibodies in combination with various cytokines, including IL-4, IL-5, IFN-gamma, and TGF-beta. B cells lacking RelB showed up to 4-fold reductions in DNA synthesis in response to LPS, CD40, and membrane Ig-dependent activation relative to controls. However, relB-/- B cells were comparable to control B cells in their ability to undergo maturation to IgM secretion and switch to the expression of IgG3, IgG1, IgG2b, IgG2a, IgE, and/or IgA under all activation conditions tested. Thus, RelB, like c-Rel and p50/NF-kappa B, plays a role in B cell proliferation. However, in contrast to c-Rel and p50/ NF-kappa B, it is not critically involved in maturation to Ig secretion or expression of Ig isotypes.


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