Cell Signaling Technology

RBBP5 (D3I6P) Rabbit Monoclonal Antibody

#13171 · $159

100
Citing papers
3.2k
Combined citations
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Research areas

Heat shock proteins research9Amyotrophic Lateral Sclerosis Research8RNA Research and Splicing7Endoplasmic Reticulum Stress and Disease7RNA modifications and cancer6Circular RNAs in diseases6Autophagy in Disease and Therapy5Adipose Tissue and Metabolism5

Papers citing this product

1
Chaperone-mediated autophagy is involved in the execution of ferroptosis
Proceedings of the National Academy of Sciences·2019·559 cit.·DOI
2
VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis
Human Molecular Genetics·2011·547 cit.·DOI
3
Melanoma cell-secreted exosomal miR-155-5p induce proangiogenic switch of cancer-associated fibroblasts via SOCS1/JAK2/STAT3 signaling pathway
Journal of Experimental & Clinical Cancer Research·2018·290 cit.·DOI
4
Inhibition of the CDK2 and Cyclin A complex leads to autophagic degradation of CDK2 in cancer cells
Nature Communications·2022·112 cit.·DOI
5
The cleavage pattern of TDP-43 determines its rate of clearance and cytotoxicity
Nature Communications·2015·112 cit.·DOI
6
Interaction of RNA with a C-terminal fragment of the amyotrophic lateral sclerosis-associated TDP43 reduces cytotoxicity
Scientific Reports·2016·85 cit.·DOI
7
Carnosol inhibits inflammasome activation by directly targeting HSP90 to treat inflammasome-mediated diseases
Cell Death and Disease·2020·80 cit.·DOI
8
An Agonist of the Protective Factor SIRT1 Improves Functional Recovery and Promotes Neuronal Survival by Attenuating Inflammation after Spinal Cord Injury
Journal of Neuroscience·2017·80 cit.·DOI
9
Cdk5 phosphorylates non-genotoxically overexpressed p53 following inhibition of PP2A to induce cell cycle arrest/apoptosis and inhibits tumor progression
Molecular Cancer·2010·60 cit.·DOI
10
Geldanamycin-induced Lyn dissociation from aberrant Hsp90-stabilized cytosolic complex is an early event in apoptotic mechanisms in B-chronic lymphocytic leukemia
Blood·2008·55 cit.·DOI

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