Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1396 | Human HGF CHO Cell Lysate | Inquiry |
CLOE-1908 | Rat Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2960 | Mouse Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2962 | Mouse Hgf (His) HEK293 Cell Lysate | Inquiry |
CSC-DC006967 | Panoply™ Human HGF Knockdown Stable Cell Line | Inquiry |
CSC-DC007610 | Panoply™ Human IL6 Knockdown Stable Cell Line | Inquiry |
CSC-DC014899 | Panoply™ Human SOS1 Knockdown Stable Cell Line | Inquiry |
CSC-RO01388 | Human IL6 Stable Cell Line - HEK293 | Inquiry |
CSC-RT2297 | Human SOS1 Knockout Cell Line-HEK293T | Inquiry |
CSC-RT2411 | Human HGF Knockout Cell Line-Hela | Inquiry |
CSC-SC006967 | Panoply™ Human HGF Over-expressing Stable Cell Line | Inquiry |
CSC-SC007610 | Panoply™ Human IL6 Over-expressing Stable Cell Line | Inquiry |
CSC-SC014899 | Panoply™ Human SOS1 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1396 | Human HGF CHO Cell Lysate | Inquiry |
CLOE-1908 | Rat Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2960 | Mouse Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2962 | Mouse Hgf (His) HEK293 Cell Lysate | Inquiry |
CSC-DC006967 | Panoply™ Human HGF Knockdown Stable Cell Line | Inquiry |
CSC-DC007610 | Panoply™ Human IL6 Knockdown Stable Cell Line | Inquiry |
CSC-DC014899 | Panoply™ Human SOS1 Knockdown Stable Cell Line | Inquiry |
CSC-RO01388 | Human IL6 Stable Cell Line - HEK293 | Inquiry |
CSC-RT2297 | Human SOS1 Knockout Cell Line-HEK293T | Inquiry |
CSC-RT2411 | Human HGF Knockout Cell Line-Hela | Inquiry |
CSC-SC006967 | Panoply™ Human HGF Over-expressing Stable Cell Line | Inquiry |
CSC-SC007610 | Panoply™ Human IL6 Over-expressing Stable Cell Line | Inquiry |
CSC-SC014899 | Panoply™ Human SOS1 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1396 | Human HGF CHO Cell Lysate | Inquiry |
CLOE-1908 | Rat Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2960 | Mouse Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2962 | Mouse Hgf (His) HEK293 Cell Lysate | Inquiry |
CSC-DC006967 | Panoply™ Human HGF Knockdown Stable Cell Line | Inquiry |
CSC-DC007610 | Panoply™ Human IL6 Knockdown Stable Cell Line | Inquiry |
CSC-DC014899 | Panoply™ Human SOS1 Knockdown Stable Cell Line | Inquiry |
CSC-RO01388 | Human IL6 Stable Cell Line - HEK293 | Inquiry |
CSC-RT2297 | Human SOS1 Knockout Cell Line-HEK293T | Inquiry |
CSC-RT2411 | Human HGF Knockout Cell Line-Hela | Inquiry |
CSC-SC006967 | Panoply™ Human HGF Over-expressing Stable Cell Line | Inquiry |
CSC-SC007610 | Panoply™ Human IL6 Over-expressing Stable Cell Line | Inquiry |
CSC-SC014899 | Panoply™ Human SOS1 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1396 | Human HGF CHO Cell Lysate | Inquiry |
CLOE-1908 | Rat Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2960 | Mouse Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2962 | Mouse Hgf (His) HEK293 Cell Lysate | Inquiry |
CSC-DC006967 | Panoply™ Human HGF Knockdown Stable Cell Line | Inquiry |
CSC-DC007610 | Panoply™ Human IL6 Knockdown Stable Cell Line | Inquiry |
CSC-DC014899 | Panoply™ Human SOS1 Knockdown Stable Cell Line | Inquiry |
CSC-RO01388 | Human IL6 Stable Cell Line - HEK293 | Inquiry |
CSC-RT2297 | Human SOS1 Knockout Cell Line-HEK293T | Inquiry |
CSC-RT2411 | Human HGF Knockout Cell Line-Hela | Inquiry |
CSC-SC006967 | Panoply™ Human HGF Over-expressing Stable Cell Line | Inquiry |
CSC-SC007610 | Panoply™ Human IL6 Over-expressing Stable Cell Line | Inquiry |
CSC-SC014899 | Panoply™ Human SOS1 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLOE-1396 | Human HGF CHO Cell Lysate | Inquiry |
CLOE-1908 | Rat Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2960 | Mouse Hgf HEK293 Cell Lysate | Inquiry |
CLOE-2962 | Mouse Hgf (His) HEK293 Cell Lysate | Inquiry |
CSC-DC006967 | Panoply™ Human HGF Knockdown Stable Cell Line | Inquiry |
CSC-DC007610 | Panoply™ Human IL6 Knockdown Stable Cell Line | Inquiry |
CSC-DC014899 | Panoply™ Human SOS1 Knockdown Stable Cell Line | Inquiry |
CSC-RO01388 | Human IL6 Stable Cell Line - HEK293 | Inquiry |
CSC-RT2297 | Human SOS1 Knockout Cell Line-HEK293T | Inquiry |
CSC-RT2411 | Human HGF Knockout Cell Line-Hela | Inquiry |
CSC-SC006967 | Panoply™ Human HGF Over-expressing Stable Cell Line | Inquiry |
CSC-SC007610 | Panoply™ Human IL6 Over-expressing Stable Cell Line | Inquiry |
CSC-SC014899 | Panoply™ Human SOS1 Over-expressing Stable Cell Line | Inquiry |
The hepatocyte growth factor (HGF) represents a remarkable example of molecular complexity in cellular signaling. First discovered in rat plasma in 1984, HGF exists as a sophisticated heterodimeric molecule comprising a 69kDa α-chain and a 34kDa β-chain. The α-chain features a distinctive hairpin structure at its N-terminus, while the β-chain contains a serine protease-like domain. Despite its structural similarity to serine proteases, HGF lacks enzymatic activity, instead functioning as a versatile signaling molecule that orchestrates numerous cellular processes.
When HGF binds to its receptor c-Met, it initiates a cascade of molecular events that begins with receptor dimerization and subsequent tyrosine phosphorylation. This activation triggers multiple downstream signaling pathways, including PI3K-AKT, Ras-MAPK, STAT, and Wnt/β-catenin cascades. Through these pathways, HGF regulates diverse cellular behaviors, from proliferation and migration to survival and morphogenesis. The protein's influence extends across various tissue types, where it acts through both paracrine and autocrine mechanisms to coordinate complex cellular responses.
Figure 1. Overview of the HGF/MET Signaling Pathway and Its Targeted Therapy. (Moosavi, F. et. al., 2021)
HGF/c-Met signaling regulates cell organization and tissue formation throughout embryonic development. The path coordinates skeletal muscle development, guides mesenchymal stem cell migration, and promotes brain tissue growth. HGF/c-Met signaling maintains adult stem cells functioning and helps to maintain the balance of numerous specialized cells, like heart muscle cells, pancreatic β cells, and hepatocytes in adult tissues, thereby continuing this function in development.
In many various methods, HGF mends injuries and repairs damaged tissues in formed tissues. By modulating fibroblast activity, the protein prevents damage from becoming too severe and promotes blood vessel formation, which enables tissues to repair by extending cell life. How well epithelial and mesenchymal tissues cooperate will determine these duties. HGF is a major driver of intercellular communication.
The role of HGF/c-Met signaling in cancer represents a compelling example of how normal physiological processes can be hijacked during disease development. Cancer cells often exploit this pathway by secreting excessive amounts of HGF into the tumor microenvironment (TME), creating a self-perpetuating cycle of growth and invasion. This process begins with cancer cells producing HGF, which activates c-Met receptors on both tumor cells and surrounding stromal cells. This leads to increased HGF production and creates a positive feedback loop that supports tumor growth.
The pathway's influence on cancer stem cells (CSCs) particularly highlights its significance in tumor progression. In pancreatic cancer, HGF/c-Met signaling helps maintain CSC populations by regulating their metabolic preferences. In colorectal cancer, the pathway drives abnormal Wnt/β-catenin signaling, promoting metastasis. Hepatocellular carcinoma shows a distinctive pattern where cancer-associated fibroblasts utilize c-Met/FRA1/HEY1 signaling to support CSC self-renewal.
HGF/c-Met signaling regulates a complex network of cell contacts in the vicinity of a tumor that supports its growth. The path is very effective in several respects for promoting angiogenesis. It raises VEGFA production and lowers the effectiveness of natural angiogenesis inhibitors such as thrombospondin 1. HGF also promotes the growth and development of vascular stem cells, which directly support the formation of new blood vessels.
The path influences more than only the development of blood vessels; it also influences how stroma and tumors interact in a larger context. Cancer-related fibroblasts produce more HGF when they detect signals from the stroma. This further alters the local environment to assist the tumor in growing. With HGF/c-Met signals being rather important, this creates a complicated situation at the molecular level where cancer cells and stromal cells communicate constantly.
Treatment has become a hot topic because HGF/c-Met signaling is so crucial in cancer. By use of many c-Met blockers including Crizotinib, this communication method has been proven to hold promise in the sector. However, given the complexity of cancer biology, treating HGF/c-Met would not be sufficient to provide the optimal outcomes from therapy.
Recent research has shown intriguing connections between HGF/c-Met signaling and how medications no longer perform as they once did. For instance, in non-small cell lung cancer, alterations in metabolism involving HGF signaling might reduce the efficacy of EGFR medications. These findings have led to the development of more sophisticated cancer treatment strategies including combination therapies that simultaneously target many pathways.
Much clinical research investigating novel treatment approaches will help the sector to evolve in the future. Some of this research seeks novel pharmaceutical choices aimed at various areas of the HGF/c-Met pathway. Others examine how this route interacts with other significant signaling networks, including EGF and VEGF. Our knowledge of these complex biological processes is helping us to move closer to more efficient and particular cancer therapies that can better address the issues of tumor diversity and drug resistance.
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