Introduction
Introduction
The Hedgehog (Hh) gene was discovered in 1980 by Nusslein Volhard and Wieschaus for genetic analysis of Drosophila melanogaster. In the early 1990s, three Hh homologous genes were found in vertebrates, namely Sonic hedgehog (Shh), Indian hedgehog (Ihh) and Desert hedgehog (Dhh). Dhh and Ihh play important roles in the development of normal tissues such as pancreas, testicular formation, and bone development. Shh is the most important member of the three and is widely expressed in adult organizations.
The Hh signaling pathway is a highly compliant signaling pathway that plays an important role in many aspects. Especially, it plays a vital role in embryonic development and growth regulation, being morphogens, mitogens and organ development inducing factors, such as cell proliferation, cell adhesion, cell migration, cell differentiation and embryogenesis. Hh signaling pathway can participate in wound healing of multiple mature organ tissues simultaneously and is one of the important factors involved in liver damage repair, but its excessive activation can lead to liver fibrosis and liver cancer. Shh has been shown to be a strong oncogene, and overexpression of Shh induces basal cell carcinoma in mice. Excessive activation of the Hh signaling pathway has been detected in a variety of solid tumors, such as medulloblastoma, leukemia, breast cancer, prostate cancer, pancreatic cancer, basal cell carcinoma, non-small cell lung cancer, and small cell lung cancer. Statistics show that up to 25% of human cancer deaths may be associated with abnormal Hh signaling pathways. Therefore, researchers need to explore the mechanism of Hh signaling pathway in more depth and find new targets for tumor-targeted therapy and inflammatory injury repair.
Figure 1. Classical canonical and proposed non-canonical Hedgehog signaling
Canonical Hh signaling pathway
The key ligands of the canonical Hh signaling pathway are Shh, Ihh, and Dhh. By autocrine, paracrine, and endocrine means, Shh binds to the receptor transmembrane protein-patch-1 (Ptch1) of the Hh signaling pathway. Thereby, the inhibition of smoothing (Smo) by Ptch1 under normal conditions is removed, and Smo can interact with related cytokines. Then, the Hh signaling pathway end effector glioma associated oncogene (Gli) family transcription factor nuclear translocation, regulation of Gli target gene expression, and finally the Hh signaling pathway is activated.
Return to Signaling Pathway
Research Areas Related Targets Featured Products
Cancer Hedgehog Vismodegib
Infection Smo MK-4101
Alzheimer's disease Akt Purmorphamine
Neurological Disease PI3K Cyclopamine
Cancer Immunotherapy Gli A-1155463
Inflammation/Immunology Caspase GANT-61
Cardiovascular and blood system Bcl-2 Family BDA-366
Endocrinology and Metabolic Disease FLT3 A-1331852
The Hedgehog (Hh) gene was discovered in 1980 by Nusslein Volhard and Wieschaus for genetic analysis of Drosophila melanogaster. In the early 1990s, three Hh homologous genes were found in vertebrates, namely Sonic hedgehog (Shh), Indian hedgehog (Ihh) and Desert hedgehog (Dhh). Dhh and Ihh play important roles in the development of normal tissues such as pancreas, testicular formation, and bone development. Shh is the most important member of the three and is widely expressed in adult organizations.
The Hh signaling pathway is a highly compliant signaling pathway that plays an important role in many aspects. Especially, it plays a vital role in embryonic development and growth regulation, being morphogens, mitogens and organ development inducing factors, such as cell proliferation, cell adhesion, cell migration, cell differentiation and embryogenesis. Hh signaling pathway can participate in wound healing of multiple mature organ tissues simultaneously and is one of the important factors involved in liver damage repair, but its excessive activation can lead to liver fibrosis and liver cancer. Shh has been shown to be a strong oncogene, and overexpression of Shh induces basal cell carcinoma in mice. Excessive activation of the Hh signaling pathway has been detected in a variety of solid tumors, such as medulloblastoma, leukemia, breast cancer, prostate cancer, pancreatic cancer, basal cell carcinoma, non-small cell lung cancer, and small cell lung cancer. Statistics show that up to 25% of human cancer deaths may be associated with abnormal Hh signaling pathways. Therefore, researchers need to explore the mechanism of Hh signaling pathway in more depth and find new targets for tumor-targeted therapy and inflammatory injury repair.
Figure 1. Classical canonical and proposed non-canonical Hedgehog signaling
Canonical Hh signaling pathway
The key ligands of the canonical Hh signaling pathway are Shh, Ihh, and Dhh. By autocrine, paracrine, and endocrine means, Shh binds to the receptor transmembrane protein-patch-1 (Ptch1) of the Hh signaling pathway. Thereby, the inhibition of smoothing (Smo) by Ptch1 under normal conditions is removed, and Smo can interact with related cytokines. Then, the Hh signaling pathway end effector glioma associated oncogene (Gli) family transcription factor nuclear translocation, regulation of Gli target gene expression, and finally the Hh signaling pathway is activated.
Return to Signaling Pathway
Research Areas Related Targets Featured Products
Cancer Hedgehog Vismodegib
Infection Smo MK-4101
Alzheimer's disease Akt Purmorphamine
Neurological Disease PI3K Cyclopamine
Cancer Immunotherapy Gli A-1155463
Inflammation/Immunology Caspase GANT-61
Cardiovascular and blood system Bcl-2 Family BDA-366
Endocrinology and Metabolic Disease FLT3 A-1331852
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