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Cell Signaling Technology
Phospho-PP1 alpha (Thr320) Antibody
#2581 · $366
100
Citing papers
17.4k
Combined citations
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Research areas
Autophagy in Disease and Therapy
15
Neurogenesis and neuroplasticity mechanisms
7
Nerve injury and regeneration
6
Epigenetics and DNA Methylation
6
MicroRNA in disease regulation
6
Immune Cell Function and Interaction
5
Immune cells in cancer
5
Mesenchymal stem cell research
5
Papers citing this product
1
The unfolded protein response protects human tumor cells during hypoxia through regulation of the autophagy genes MAP1LC3B and ATG5
Journal of Clinical Investigation
·
2009
·
799 cit.
·
DOI
2
DUSP1 alleviates cardiac ischemia/reperfusion injury by suppressing the Mff-required mitochondrial fission and Bnip3-related mitophagy via the JNK pathways
Redox Biology
·
2017
·
459 cit.
·
DOI
3
Genetic absence of PD-1 promotes accumulation of terminally differentiated exhausted CD8+ T cells
The Journal of Experimental Medicine
·
2015
·
452 cit.
·
DOI
4
Tumor Necrosis Factor-α Stimulates Lipolysis in Differentiated Human Adipocytes Through Activation of Extracellular Signal-Related Kinase and Elevation of Intracellular cAMP
Diabetes
·
2002
·
423 cit.
·
DOI
5
Autophagy promotes the survival of dormant breast cancer cells and metastatic tumour recurrence
Nature Communications
·
2018
·
418 cit.
·
DOI
6
Radiosensitization and DNA repair inhibition by the combined use of novel inhibitors of DNA-dependent protein kinase and poly(ADP-ribose) polymerase-1.
PubMed
·
2003
·
331 cit.
7
BRCA locus-specific loss of heterozygosity in germline BRCA1 and BRCA2 carriers
Nature Communications
·
2017
·
308 cit.
·
DOI
8
Bnip3 impairs mitochondrial bioenergetics and stimulates mitochondrial turnover
Cell Death and Differentiation
·
2010
·
291 cit.
·
DOI
9
PS1 activates PI3K thus inhibiting GSK‐3 activity and tau overphosphorylation: effects of FAD mutations
The EMBO Journal
·
2004
·
287 cit.
·
DOI
10
Diabetes-Induced Oxidative Stress and Low-Grade Inflammation in Porcine Coronary Arteries
Circulation
·
2003
·
283 cit.
·
DOI
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