Browsing by Author "Kim, Taesoo"

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    Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway
    (eLife Sciences Publications, 2021-08-06) Kweon, Hyae Yon; Lee, Mi-Ni; Dorfel, Max; Seo, Seungwoon; Gottlieb, Leah; PaPazyan, Thomas; McTiernan, Nina; Ree, Rasmus; Bolton, David; Garcia, Andrew; Flory, Michael; Crain, Jonathan; Sebold, Alison; Lyons, Scott; Ismail, Ahmed; Marchi, Elaine; Sonn, Seong-keun; Jeong, Se-Jin; Jeon, Sejin; Ju, Shinyeong; Conway, Simon J.; Kim, Taesoo; Kim, Hyun-Seok; Lee, Cheolju; Roh, Tae-Young; Arnesen, Thomas; Marmorstein, Ronen; Oh, Goo Taeg; Lyon, Gholson J.; Pediatrics, School of Medicine
    Amino-terminal acetylation is catalyzed by a set of N-terminal acetyltransferases (NATs). The NatA complex (including X-linked Naa10 and Naa15) is the major acetyltransferase, with 40-50% of all mammalian proteins being potential substrates. However, the overall role of amino-terminal acetylation on a whole-organism level is poorly understood, particularly in mammals. Male mice lacking Naa10 show no globally apparent in vivo amino-terminal acetylation impairment and do not exhibit complete embryonic lethality. Rather Naa10 nulls display increased neonatal lethality, and the majority of surviving undersized mutants exhibit a combination of hydrocephaly, cardiac defects, homeotic anterior transformation, piebaldism, and urogenital anomalies. Naa12 is a previously unannotated Naa10-like paralog with NAT activity that genetically compensates for Naa10. Mice deficient for Naa12 have no apparent phenotype, whereas mice deficient for Naa10 and Naa12 display embryonic lethality. The discovery of Naa12 adds to the currently known machinery involved in amino-terminal acetylation in mice.
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    Plasma proteomics of acute tubular injury
    (Springer Nature, 2024-08-27) Schmidt, Insa M.; Surapaneni, Aditya L.; Zhao, Runqi; Upadhyay, Dhairya; Yeo, Wan-Jin; Schlosser, Pascal; Huynh, Courtney; Srivastava, Anand; Palsson, Ragnar; Kim, Taesoo; Stillman, Isaac E.; Barwinska, Daria; Barasch, Jonathan; Eadon, Michael T.; El-Achkar, Tarek M.; Henderson, Joel; Moledina, Dennis G.; Rosas, Sylvia E.; Claudel, Sophie E.; Verma, Ashish; Wen, Yumeng; Lindenmayer, Maja; Huber, Tobias B.; Parikh, Samir V.; Shapiro, John P.; Rovin, Brad H.; Stanaway, Ian B.; Sathe, Neha A.; Bhatraju, Pavan K.; Coresh, Josef; Kidney Precision Medicine Project; Rhee, Eugene P.; Grams, Morgan E.; Waikar, Sushrut S.; Medicine, School of Medicine
    The kidney tubules constitute two-thirds of the cells of the kidney and account for the majority of the organ’s metabolic energy expenditure. Acute tubular injury (ATI) is observed across various types of kidney diseases and may significantly contribute to progression to kidney failure. Non-invasive biomarkers of ATI may allow for early detection and drug development. Using the SomaScan proteomics platform on 434 patients with biopsy-confirmed kidney disease, we here identify plasma biomarkers associated with ATI severity. We employ regional transcriptomics and proteomics, single-cell RNA sequencing, and pathway analysis to explore biomarker protein and gene expression and enriched biological pathways. Additionally, we examine ATI biomarker associations with acute kidney injury (AKI) in the Kidney Precision Medicine Project (KPMP) (n = 44), the Atherosclerosis Risk in Communities (ARIC) study (n = 4610), and the COVID-19 Host Response and Clinical Outcomes (CHROME) study (n = 268). Our findings indicate 156 plasma proteins significantly linked to ATI with osteopontin, macrophage mannose receptor 1, and tenascin C showing the strongest associations. Pathway analysis highlight immune regulation and organelle stress responses in ATI pathogenesis.