Cell Signaling Technology

Progesterone Receptor A/B (D8Q2J) Rabbit Monoclonal Antibody

#8757 · $161

100
Citing papers
5.6k
Combined citations
Supplier page Find this product

Research areas

Reproductive System and Pregnancy9Estrogen and related hormone effects8Ubiquitin and proteasome pathways8Cancer Cells and Metastasis7Cancer-related Molecular Pathways6Neuroscience and Neuropharmacology Research6Adipose Tissue and Metabolism5Cancer, Hypoxia, and Metabolism5

Papers citing this product

1
Analytical Modeling in Applied Electromagnetics
Medical Entomology and Zoology·2003·940 cit.·DOI
2
Acquired CDK6 amplification promotes breast cancer resistance to CDK4/6 inhibitors and loss of ER signaling and dependence
Oncogene·2016·430 cit.·DOI
3
Targeting of Interferon-Beta to Produce a Specific, Multi-Mechanistic Oncolytic Vaccinia Virus
PLoS Medicine·2007·202 cit.·DOI
4
Rational strain selection and engineering creates a broad-spectrum, systemically effective oncolytic poxvirus, JX-963
Journal of Clinical Investigation·2007·198 cit.·DOI
5
Mitochondria contribute to LPS-induced MAPK activation via uncoupling protein UCP2 in macrophages
Biochemical Journal·2007·162 cit.·DOI
6
The Calcium Channel α<sub>2</sub>δ-2 Subunit Partitions with Ca<sub>V</sub>2.1 into Lipid Rafts in Cerebellum: Implications for Localization and Function
Journal of Neuroscience·2006·157 cit.·DOI
7
Oral Estrogen Receptor PROTAC Vepdegestrant (ARV-471) Is Highly Efficacious as Monotherapy and in Combination with CDK4/6 or PI3K/mTOR Pathway Inhibitors in Preclinical ER+ Breast Cancer Models
Clinical Cancer Research·2024·152 cit.·DOI
8
Natural Product Micheliolide (MCL) Irreversibly Activates Pyruvate Kinase M2 and Suppresses Leukemia
Journal of Medicinal Chemistry·2018·149 cit.·DOI
9
KMT2C mediates the estrogen dependence of breast cancer through regulation of ERα enhancer function
Oncogene·2018·149 cit.·DOI
10
Inactivating <i>NF1</i> Mutations Are Enriched in Advanced Breast Cancer and Contribute to Endocrine Therapy Resistance
Clinical Cancer Research·2019·136 cit.·DOI

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