Iron‐stress response mechanism and iron uptake in iron‐efficient and ‐inefficient tomatoes and soybeans treated with cobalt

1985 ◽  
Vol 8 (2) ◽  
pp. 163-176 ◽  
Author(s):  
A.D. Blaylock ◽  
V.D. Jolley ◽  
J.C. Brown ◽  
T.D. Davis ◽  
R.H. Walser
Keyword(s):  
Stress Response ◽  
Iron Uptake ◽  
Iron Stress ◽  
Response Mechanism

Iron‐stress response mechanism and iron uptake in iron‐efficient and‐ inefficient tomatoes and soybeans treated with cobalt

1985 ◽  
Vol 8 (1) ◽  
pp. 1-14 ◽  
Author(s):  
A.D. Blaylock ◽  
V.D. Jolley ◽  
J.C. Brown ◽  
T.D. Davis ◽  
R.H. Walser
Keyword(s):  
Stress Response ◽  
Iron Uptake ◽  
Iron Stress ◽  
Response Mechanism

The role of active Bradyrhizobium japonicum in iron stress response of soybeans

1991 ◽  
Vol 130 (1-2) ◽  
pp. 225-230 ◽  
Author(s):  
R. E. Terry ◽  
K. U. Soerensen ◽  
D. Von Jolley ◽  
J. C. Brown
Keyword(s):  
Stress Response ◽  
Bradyrhizobium Japonicum ◽  
Iron Stress

scholarly journals Nrf1 promotes heart regeneration and repair by regulating proteostasis and redox balance

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Miao Cui ◽  
Ayhan Atmanli ◽  
Maria Gabriela Morales ◽  
Wei Tan ◽  
Kenian Chen ◽  
...  
Keyword(s):  
Stress Response ◽  
Ischemia Reperfusion ◽  
Induced Pluripotent Stem Cell ◽  
Redox Balance ◽  
Mouse Heart ◽  
Heart Regeneration ◽  
Response Mechanism ◽  
Protective Function ◽  
Neonatal Heart ◽  
Induced Pluripotent

AbstractFollowing injury, cells in regenerative tissues have the ability to regrow. The mechanisms whereby regenerating cells adapt to injury-induced stress conditions and activate the regenerative program remain to be defined. Here, using the mammalian neonatal heart regeneration model, we show that Nrf1, a stress-responsive transcription factor encoded by the Nuclear Factor Erythroid 2 Like 1 (Nfe2l1) gene, is activated in regenerating cardiomyocytes. Genetic deletion of Nrf1 prevented regenerating cardiomyocytes from activating a transcriptional program required for heart regeneration. Conversely, Nrf1 overexpression protected the adult mouse heart from ischemia/reperfusion (I/R) injury. Nrf1 also protected human induced pluripotent stem cell-derived cardiomyocytes from doxorubicin-induced cardiotoxicity and other cardiotoxins. The protective function of Nrf1 is mediated by a dual stress response mechanism involving activation of the proteasome and redox balance. Our findings reveal that the adaptive stress response mechanism mediated by Nrf1 is required for neonatal heart regeneration and confers cardioprotection in the adult heart.

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