Cell Signaling Technology

Bora (D2B9) Rabbit Monoclonal Antibody

#12109 · western blot · $161,351

63

Evidence Score · Well-Established

Used by 96 independent labs across 100 papers. How we score this →

100

Citing papers

5.8k

Combined citations

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Research areas

Autophagy in Disease and Therapy24 Calcium signaling and nucleotide metabolism18 Muscle Physiology and Disorders17 Extracellular vesicles in disease7 Mitochondrial Function and Pathology6 Mesenchymal stem cell research6 Muscle metabolism and nutrition5 Growth Hormone and Insulin-like Growth Factors4

Papers citing this product

1

MCOLN1 is a ROS sensor in lysosomes that regulates autophagy

Nature Communications·2016·549 cit.·DOI

2

Activation of mitochondrial TUFM ameliorates metabolic dysregulation through coordinating autophagy induction

Communications Biology·2021·332 cit.·DOI

3

Mesenchymal stromal cell apoptosis is required for their therapeutic function

Nature Communications·2021·254 cit.·DOI

4

Sphingosylphosphorylcholine and Lysophosphatidylcholine Are Ligands for the G Protein-coupled Receptor GPR4

Journal of Biological Chemistry·2001·241 cit.·DOI

5

Metformin induces cell cycle arrest, apoptosis and autophagy through ROS/JNK signaling pathway in human osteosarcoma

International Journal of Biological Sciences·2019·191 cit.·DOI

6

Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids

Journal of Clinical Investigation·2002·174 cit.·DOI

7

Insulin-Like Growth Factor-1 Receptor Is Regulated by microRNA-133 during Skeletal Myogenesis

PLoS ONE·2011·166 cit.·DOI

8

Mitochondrial ROS-induced lysosomal dysfunction impairs autophagic flux and contributes to M1 macrophage polarization in a diabetic condition

Clinical Science·2019·153 cit.·DOI

9

TRIP13 promotes error-prone nonhomologous end joining and induces chemoresistance in head and neck cancer

Nature Communications·2014·152 cit.·DOI

10

Losing Control: Excessive Alcohol Seeking after Selective Inactivation of Cue-Responsive Neurons in the Infralimbic Cortex

Journal of Neuroscience·2015·149 cit.·DOI

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