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    LH1 and SEPT2 are overexpressed in several cancers including hepatocellular carcinoma, pancreatic ductal adenocarcinoma, and breast cancer. A genetic duplication and mutations in PLOD1 cause Ehlers-Danlos syndrome type VIA by disrupting the hydroxylation of collagen through reduced activity of LH1. Hypoxia-inducible factor 1 activates LH1 upregulation and contributes to hereditary thoracic aortic disease when LH1 has a missense variant.

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    LH1 and SEPT2 are overexpressed in several cancers including hepatocellular carcinoma, pancreatic ductal adenocarcinoma, and breast cancer. A genetic duplication and mutations in PLOD1 cause Ehlers-Danlos syndrome type VIA by disrupting the hydroxylation of collagen through reduced activity of LH1. Hypoxia-inducible factor 1 activates LH1 upregulation and contributes to hereditary thoracic aortic disease when LH1 has a missense variant.

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    Pathway

    Uploaded by

    Mehwsih
    LH1 and SEPT2 are overexpressed in several cancers including hepatocellular carcinoma, pancreatic ductal adenocarcinoma, and breast cancer. A genetic duplication and mutations in PLOD1 cause Ehlers-Danlos syndrome type VIA by disrupting the hydroxylation of collagen through reduced activity of LH1. Hypoxia-inducible factor 1 activates LH1 upregulation and contributes to hereditary thoracic aortic disease when LH1 has a missense variant.

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    of 2

    PDAC (Pancreatic

    HCC Ductal
    (Hepatocellular Adenocarcinoma) EDS type VIA
    Carcinoma)
    Overexpressed. LH1
    & SEPT2 Correlation
    Overexpressed. LH1 Duplication of exon 10 to exon 16 and
    & SEPT2 Correlation two mutation on Gln208 & Tyr675 cause
    the loss function of PLOD1. PLOD1
    LH1 (Lysyl regulates the hydroxylation of lysyl
    residues on collagen type V
    hydroxylase 1)
    HIF-1 activates LH1
    (PLOD1) upregulation
    Missense p.
    HTAD (Heritable (Ser178Arg variant)
    thoracic aortic Breast Cancer
    disease)

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