MAPK/ERK Signaling Pathway Research Reagents

The MAPK/ERK (Ras-Raf-MEK-ERK) pathway is a central mitogenic signaling cascade that transduces extracellular growth factor signals into cell proliferation, differentiation, survival, and migration responses. Receptor tyrosine kinase (RTK) activation by ligands such as EGF, FGF, or PDGF triggers RAS GTPase loading, which recruits and activates the RAF serine/threonine kinases (ARAF, BRAF, CRAF). RAF phosphorylates and activates MEK1/2 (dual-specificity kinases), which in turn phosphorylate ERK1/2 (MAPK3/1). Activated ERK1/2 translocate to the nucleus and phosphorylate transcription factors including ELK1, MYC, and RSK family members to drive cell cycle progression. Oncogenic mutations in this pathway — particularly KRAS (G12/G13/Q61), BRAF (V600E), and NF1 loss — are among the most frequent drivers across human cancers, making the MAPK/ERK cascade one of the most therapeutically targeted signaling axes in oncology.

Research Use Only (RUO)Not intended for diagnostic or therapeutic procedures.

abinScience provides recombinant proteins and antibodies for key MAPK/ERK signaling targets — growth factor ligands, receptor tyrosine kinases, RAS/RAF/MEK/ERK core cascade components, and pathway regulators. Available in His-tag, Fc-tag, and biotin-conjugated formats. All products are manufactured by our parent company AtaGenix Laboratories under ISO quality systems. Browse products below or contact us for custom development.

Growth Factor Ligands & Receptor Tyrosine Kinases

EGF (Epidermal Growth Factor) — A canonical activator of the EGFR/RAS/MAPK axis. Recombinant EGF is routinely used to stimulate ERK1/2 phosphorylation in signaling studies, cell proliferation assays, and organoid culture media. EGF-induced EGFR activation also cross-talks with PI3K/AKT and JAK/STAT pathways.
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EGFR (HER1/ErbB1) — The prototypical RTK that initiates RAS/MAPK signaling upon EGF-family ligand binding. EGFR is overexpressed or mutationally activated in non-small cell lung cancer (NSCLC), glioblastoma, and colorectal cancer. EGFR is a major therapeutic target for tyrosine kinase inhibitors (erlotinib, osimertinib) and monoclonal antibodies (cetuximab).
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HER2 (ErbB2) — An orphan RTK that forms heterodimers with other ErbB family members to potently activate RAS/MAPK and PI3K signaling. HER2 gene amplification drives approximately 15–20% of breast cancers and a subset of gastric and gastroesophageal cancers. HER2 is the target of trastuzumab and HER2-directed antibody-drug conjugates.
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FGF2 (bFGF) — A pleiotropic growth factor that signals through FGFR1–4 to activate RAS/MAPK, PI3K, and PLCγ pathways. FGF2 promotes angiogenesis, wound repair, and neural stem cell maintenance. Recombinant FGF2 is a standard supplement in embryonic and induced pluripotent stem cell (iPSC) culture media.
→ Browse FGF2 antibodies & proteins

RAS/RAF/MEK/ERK Core Cascade

KRAS — A small GTPase that acts as a molecular switch at the apex of the MAPK cascade. KRAS is the most frequently mutated oncogene in human cancer, with activating mutations (G12C, G12D, G12V, G13D, Q61H) prevalent in pancreatic ductal adenocarcinoma (~90%), non-small cell lung cancer (~30%), and colorectal cancer (~40%). The approval of KRAS G12C-selective inhibitors (sotorasib, adagrasib) has validated KRAS as a druggable target after decades of being considered “undruggable.”
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BRAF — A serine/threonine kinase directly downstream of RAS. The BRAF V600E mutation constitutively activates MEK/ERK signaling and is found in ~50% of melanomas, ~60% of papillary thyroid carcinomas, and a subset of colorectal cancers and hairy cell leukemia. Vemurafenib and dabrafenib are selective BRAF V600E inhibitors used in clinical practice, typically in combination with MEK inhibitors to overcome paradoxical MAPK reactivation.
→ Browse BRAF antibodies & proteins

MEK1/2 (MAP2K1/2) — Dual-specificity kinases that serve as the obligate and sole substrates of RAF kinases, and the only direct activators of ERK1/2. This narrow specificity makes MEK a favorable pharmacological node; MEK inhibitors (trametinib, cobimetinib, selumetinib) are approved for melanoma, NSCLC, and neurofibromatosis type 1. Phospho-MEK1/2 antibodies provide a readout for RAF kinase activity.
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ERK1/2 (MAPK3/1) — The terminal kinases of the core cascade. ERK1/2 phosphorylate over 200 cytoplasmic and nuclear substrates, driving cell cycle entry (Cyclin D1), survival (RSK→BAD), and transcription factor activation (ELK1, FOS). Phospho-ERK1/2 (Thr202/Tyr204) is the most widely used readout for MAPK pathway activation across Western blot, IHC, flow cytometry, and high-content imaging platforms.
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Pathway Regulators & Feedback Modulators

SOS1 — A RAS guanine nucleotide exchange factor (GEF) that catalyzes GDP-to-GTP exchange on RAS, coupling upstream RTK activation to RAS signaling. SOS1 inhibitors are an emerging therapeutic strategy that disrupts RAS activation independently of specific RAS mutations.
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NF1 (Neurofibromin) — A RAS GTPase-activating protein (GAP) that accelerates GTP hydrolysis, returning RAS to its inactive GDP-bound state. NF1 loss-of-function mutations cause neurofibromatosis type 1 and result in constitutive RAS/MAPK activation. NF1 inactivation is also a mechanism of acquired resistance to RAF and MEK inhibitors in melanoma.
→ Browse NF1 antibodies & proteins

DUSP6 (MKP-3) — A dual-specificity phosphatase that selectively dephosphorylates and inactivates ERK1/2, providing critical negative feedback within the MAPK cascade. DUSP6 is transcriptionally induced by ERK signaling itself, forming an autoregulatory loop. Loss of DUSP6 expression has been reported in pancreatic cancer and is associated with sustained ERK activation.
→ Browse DUSP6 antibodies & proteins

References

1. Lavoie H, Gagnon J, Bhatt DK, et al. Regulation of RAF protein kinases in ERK signalling. Nat Rev Mol Cell Biol. 2015;16(5):281-298. DOI

2. Prior IA, Hood FE, Hartley JL. The frequency of Ras mutations in cancer. Cancer Res. 2020;80(14):2969-2974. DOI

3. Davies H, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949-954. DOI

4. Caunt CJ, et al. MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road. Nat Rev Cancer. 2015;15(10):577-592. DOI