<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bortoletto AS</submitter><funding>Eleanor Schwartz Charitable Trust</funding><funding>Baylor College of Medicine Medical Scientist Training Program</funding><funding>NICHD NIH HHS</funding><funding>NHLBI Division of Intramural Research</funding><funding>National Heart, Lung, and Blood Institute</funding><funding>NHLBI NIH HHS</funding><funding>National Institutes of Health</funding><funding>Mike Hogg Fund</funding><funding>NIDDK NIH HHS</funding><funding>Small Business Innovation Research</funding><funding>Robertson Therapeutic Development Fund</funding><funding>National Institute of Child Health and Human Development</funding><funding>NIH HHS</funding><pagination>e2202342</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9731688</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(34)</volume><pubmed_abstract>Type 2 diabetes mellitus (T2D) is a major public health concern and is characterized by sustained hyperglycemia due to insulin resistance and destruction of insulin-producing β cells. One pathological hallmark of T2D is the toxic accumulation of human islet amyloid polypeptide (hIAPP) aggregates. Monomeric hIAPP is a hormone normally co-secreted with insulin. However, increased levels of hIAPP in prediabetic and diabetic patients can lead to the formation of hIAPP protofibrils, which are toxic to β cells. Current therapies fail to address hIAPP aggregation and current screening modalities do not detect it. Using a stabilizing capping protein, monoclonal antibodies (mAbs) can be developed against a previously nonisolatable form of hIAPP protofibrils, which are protofibril specific and do no</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>Human Islet Amyloid Polypeptide (hIAPP) Protofibril-Specific Antibodies for Detection and Treatment of Type 2 Diabetes.</pubmed_title><pmcid>PMC9731688</pmcid><funding_grant_id>SBIR R43DK125161</funding_grant_id><funding_grant_id>R43DK125161</funding_grant_id><funding_grant_id>R43 DK125161</funding_grant_id><funding_grant_id>T32 HL092332</funding_grant_id><funding_grant_id>R01HD099252</funding_grant_id><funding_grant_id>R01HD098131</funding_grant_id><funding_grant_id>R01 HD098131</funding_grant_id><funding_grant_id>R01 HD099252</funding_grant_id><pubmed_authors>Trout G</pubmed_authors><pubmed_authors>Bonito-Oliva A</pubmed_authors><pubmed_authors>Kazmi MA</pubmed_authors><pubmed_authors>Houser BL</pubmed_authors><pubmed_authors>Sakmar TP</pubmed_authors><pubmed_authors>Parchem RJ</pubmed_authors><pubmed_authors>Weyburne E</pubmed_authors><pubmed_authors>Bortoletto AS</pubmed_authors><pubmed_authors>Gong J</pubmed_authors><pubmed_authors>Graham WV</pubmed_authors></additional><is_claimable>false</is_claimable><name>Human Islet Amyloid Polypeptide (hIAPP) Protofibril-Specific Antibodies for Detection and Treatment of Type 2 Diabetes.</name><description>Type 2 diabetes mellitus (T2D) is a major public health concern and is characterized by sustained hyperglycemia due to insulin resistance and destruction of insulin-producing β cells. One pathological hallmark of T2D is the toxic accumulation of human islet amyloid polypeptide (hIAPP) aggregates. Monomeric hIAPP is a hormone normally co-secreted with insulin. However, increased levels of hIAPP in prediabetic and diabetic patients can lead to the formation of hIAPP protofibrils, which are toxic to β cells. Current therapies fail to address hIAPP aggregation and current screening modalities do not detect it. Using a stabilizing capping protein, monoclonal antibodies (mAbs) can be developed against a previously nonisolatable form of hIAPP protofibrils, which are protofibril specific and do no</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-07-14T16:57:17.033Z</modification><creation>2026-06-21T03:07:51.258Z</creation></dates><accession>S-EPMC9731688</accession><cross_references><pubmed>36257905</pubmed><doi>10.1002/advs.202202342</doi></cross_references></HashMap>