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Anti-PORCN Antibody, clone 15G12.1 is an antibody against PORCN for use in WB & IC.
More>>Anti-PORCN Antibody, clone 15G12.1 is an antibody against PORCN for use in WB & IC. Less<<
Anti-PORCN Antibody, clone 15G12.1: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
PORCN is a multi-pass endoplasmic reticulum protein involved in the processing of wingless and other Wnt proteins that facilitate their secretion from Wnt-producing cells. Studies have shown mutations in the genes that encode for PORCN cause a pleiotropic X-linked dominant disorder, focal dermal hypolasia (FDH, also known as Goltz syndrome). Skeletal abnormalities such as syndactyly, ectordactyly, and brachydactyly, and some cases of osteopathia striata have also been attibuted to PORCN abnormalities.
References
Product Information
Format
Purified
Control
Mouse brain tissue lysate
Presentation
Purified mouse monoclonal IgMκ in buffer containing PBS with 0.05% sodium azide.
This gene belongs to the evolutionarily conserved porcupine (Porc) gene family. Genes of the Porc family encode endoplasmic reticulum proteins with multiple transmembrane domains. Porcupine proteins are involved in the processing of Wnt (wingless and int homologue) proteins. Multiple alternatively spliced transcript variants encoding distinct isoforms have been observed. [provided by RefSeq, Jul 2008].
FUNCTION: Modulates the processing of Wnt proteins. Probable protein-cysteine N-palmitoyltransferase that palmitoylates Wnt family members.
SUBUNIT STRUCTURE: Interacts with WNT1, WNT3, WNT3A, WNT4, WNT5A, WNT5B, WNT6, WNT7A and WNT7B (By similarity).
SUBCELLULAR LOCATION: Endoplasmic reticulum membrane; Multi-pass membrane protein (By similarity).
TISSUE SPECIFICITY: Isoform 1 is expressed in fetal brain, brain, amygdala, caudate nucleus, cerebellum, hippocampus, pituitary, thalamus, heart, skeletal muscle and testis. Isoform 4 is expressed in amygdala, corpus callosum, hippocampus, spinal cord, kidney, liver, lung, spleen, uterus, testis. Isoform 2 and isoform 3 are expressed in substantia negra, spinal cord, heart and lung.
INVOLVEMENT IN DISEASE: Defects in PORCN are the cause of focal dermal hypoplasia (FODH) [MIM:305600]; also known as Goltz Gorlin syndrome. A rare congenital ectomesodermal disorder characterized by a combination of skin defects, skeletal abnormalities, and ocular anomalies. Affected individuals have patchy dermal hypoplasia, often in a distribution pattern following the Blaschko lines, and areas of subcutaneous fat herniation or deposition of fat into the dermis. In addition, sparse and brittle hair, hypoplastic nails and papillomas have been described. Skeletal abnormalities usually comprise syndactyly, ectrodactyly, and brachydactyly, and in some cases osteopathia striata has been seen. Patients frequently have ocular anomalies, including microphthalmia/ anophthalmia, coloboma, pigmentary and vascularization defects of the retina. Dental abnormalities are often present.
SEQUENCE SIMILARITIES: Belongs to the membrane-bound acyltransferase family. Porcupine subfamily.
SEQUENCE CAUTION: The sequence AAA74510.1 differs from that shown. Reason: The sequence differs from that shown upstream of position 63 for unknown reasons.
Molecular Weight
~62 kDa observed. Calculated molecular weight of 52 kDa. The actual MW should be observed at ~45-65 kDa. Helical membrane protein migration on SDS-PAGE may not exactly correlate with the calculated molecular weights (PNAS, 2009, 106:1760-1765).
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Quality Assurance
Evaluated by Western Blot in mouse brain tissue lysate.
Western Blot Analysis: A 1:1,000 dilution of this antibody detected PORCN in 10 µg of mouse brain tissue lysate.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Hepatocellular carcinoma (HCC) is the second-leading cause of cancer-related death worldwide, and the factors influencing HCC progression are poorly understood. Here we reveal that HCC progression via induction of epithelial-mesenchymal transition (EMT) is closely associated with the expression of CD36/fatty acid translocase and elevated free fatty acid (FFA) levels. Although obesity is manifested as elevated FFA levels, the degree of EMT was not associated with the body mass index of the patients, highlighting the specific roles of CD36 and FFA uptake. Treatment of human liver cancer cell lines with FFAs exacerbated the EMT phenotype, whereas chemical inhibition of CD36 mitigated these effects. Furthermore, the Wnt and TGF-β signaling pathways were activated upon FFA treatment, potentially acting as upstream activators of the EMT program. These results provide the first direct evidence associating CD36 and elevated FFAs with HCC progression.