<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ames HM</submitter><funding>NCI NIH HHS</funding><pagination>2113-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3174286</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>131(10)</volume><pubmed_abstract>Merkel cell carcinoma (MCC) is a neoplasm thought to originate from the neuroendocrine Merkel cells of the skin. Although the prevalence of MCC has been increasing, treatments for this disease remain limited because of a paucity of information regarding MCC biology. We have found that the endocytic oncoprotein Huntingtin-interacting protein 1 (HIP1) is expressed at high levels in ∼90% of MCC tumors and serves as a more reliable histological cytoplasmic stain than the gold standard, cytokeratin 20. Furthermore, high anti-HIP1 antibody reactivity in the sera of a cohort of MCC patients predicts the presence of metastases. Another protein that is frequently expressed at high levels in MCC tumors is the stem cell factor (SCF) receptor tyrosine kinase, c-Kit. In working toward an understanding of how HIP1 might contribute to MCC tumorigenesis, we have discovered that HIP1 interacts with SCF-activated c-Kit. These data not only identify HIP1 as a molecular marker for management of MCC patients but also show that HIP1 interacts with and slows the degradation of c-Kit.</pubmed_abstract><journal>The Journal of investigative dermatology</journal><pubmed_title>Huntingtin-interacting protein 1: a Merkel cell carcinoma marker that interacts with c-Kit.</pubmed_title><pmcid>PMC3174286</pmcid><funding_grant_id>P30 CA046592</funding_grant_id><funding_grant_id>R01 CA098730-01</funding_grant_id><funding_grant_id>R01 CA082363-01A1</funding_grant_id><funding_grant_id>R01 CA087837</funding_grant_id><funding_grant_id>R01 CA82363-03</funding_grant_id><funding_grant_id>R01 CA098730-05A1</funding_grant_id><funding_grant_id>R01 CA098730</funding_grant_id><funding_grant_id>R01 CA082363</funding_grant_id><pubmed_authors>Ross TS</pubmed_authors><pubmed_authors>Ames HM</pubmed_authors><pubmed_authors>Bichakjian CK</pubmed_authors><pubmed_authors>Verhaegen ME</pubmed_authors><pubmed_authors>Dlugosz AA</pubmed_authors><pubmed_authors>Liu GY</pubmed_authors><pubmed_authors>Fullen DR</pubmed_authors><pubmed_authors>Johnson TM</pubmed_authors><pubmed_authors>Oravecz-Wilson KI</pubmed_authors></additional><is_claimable>false</is_claimable><name>Huntingtin-interacting protein 1: a Merkel cell carcinoma marker that interacts with c-Kit.</name><description>Merkel cell carcinoma (MCC) is a neoplasm thought to originate from the neuroendocrine Merkel cells of the skin. Although the prevalence of MCC has been increasing, treatments for this disease remain limited because of a paucity of information regarding MCC biology. We have found that the endocytic oncoprotein Huntingtin-interacting protein 1 (HIP1) is expressed at high levels in ∼90% of MCC tumors and serves as a more reliable histological cytoplasmic stain than the gold standard, cytokeratin 20. Furthermore, high anti-HIP1 antibody reactivity in the sera of a cohort of MCC patients predicts the presence of metastases. Another protein that is frequently expressed at high levels in MCC tumors is the stem cell factor (SCF) receptor tyrosine kinase, c-Kit. In working toward an understanding of how HIP1 might contribute to MCC tumorigenesis, we have discovered that HIP1 interacts with SCF-activated c-Kit. These data not only identify HIP1 as a molecular marker for management of MCC patients but also show that HIP1 interacts with and slows the degradation of c-Kit.</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Oct</publication><modification>2024-11-09T09:49:53.119Z</modification><creation>2019-03-27T00:44:00Z</creation></dates><accession>S-EPMC3174286</accession><cross_references><pubmed>21697888</pubmed><doi>10.1038/jid.2011.171</doi></cross_references></HashMap>