Cell Signaling Technology

Phospho-MEK1/2 (Ser217/221) (41G9) Rabbit Monoclonal Antibody

#9154 · western blot · $168,989

65
Evidence Score · Well-Established
Used by 284 independent labs across 304 papers. How we score this →
100
Citing papers
8.3k
Combined citations
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Research areas

Ubiquitin and proteasome pathways10Melanoma and MAPK Pathways8Autophagy in Disease and Therapy6Cancer Mechanisms and Therapy6PI3K/AKT/mTOR signaling in cancer6Cancer-related Molecular Pathways5Epigenetics and DNA Methylation4Histone Deacetylase Inhibitors Research4

Papers citing this product

1
Rheb Binds Tuberous Sclerosis Complex 2 (TSC2) and Promotes S6 Kinase Activation in a Rapamycin- and Farnesylation-dependent Manner
Journal of Biological Chemistry·2003·383 cit.·DOI
2
SAMHD1 restricts HIV-1 reverse transcription in quiescent CD4+T-cells
Retrovirology·2012·319 cit.·DOI
3
Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms
Nature Medicine·2019·228 cit.·DOI
4
RASA2 ablation in T cells boosts antigen sensitivity and long-term function
Nature·2022·219 cit.·DOI
5
Chemotherapy-related cachexia is associated with mitochondrial depletion and the activation of ERK1/2 and p38 MAPKs
Oncotarget·2016·196 cit.·DOI
6
Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis
Frontiers in Cellular and Infection Microbiology·2017·176 cit.·DOI
7
Cancer drug addiction is relayed by an ERK2-dependent phenotype switch
Nature·2017·161 cit.·DOI
8
CAF-secreted CXCL1 conferred radioresistance by regulating DNA damage response in a ROS-dependent manner in esophageal squamous cell carcinoma
Cell Death and Disease·2017·151 cit.·DOI
9
Increased glucose tolerance and reduced adiposity in the absence of fasting hypoglycemia in mice with liver-specific Gsα deficiency
Journal of Clinical Investigation·2005·144 cit.·DOI
10
Recurrent hotspot mutations in HRAS Q61 and PI3K-AKT pathway genes as drivers of breast adenomyoepitheliomas
Nature Communications·2018·138 cit.·DOI

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