Nicolas Pintozzi

PhD Student in the Blum Research Group

Mechanisms of compensatory islet expansion in Down syndrome

Nicolas has a B.S. in Biology from Case Western Reserve University. When he’s not in the lab, you can find Nicolas at the campus pottery studio, tending to his succulents, or out with friends.

npintozzi@wisc.edu

Website

Type: Graduate Student

Stromal and Neuronal Sources of Slit2/3 Ligands in the Adult Pancreas Exhibit Distinct Expression Patterns Independent of Robo2 Receptor Expression in the Islet

Matthew R Wagner, Nicolas G Pintozzi, Bjorn M Schoff, Marissa I Gold, Rachel H Kasper, Nina G Steele, Barak Blum

bioRxiv : the preprint server for biology. 2026 June 4.
Genome-wide cell type-specific and sex-specific transcriptional dysregulation in the islet of Langerhans underlies islet dysfunction in Down syndrome-related diabetes

Cyrus R Sethna, Mendoza Niemes Maria Del Carmen, Bayley J Waters, Matthew R Wagner, Jacob M Smith, Sutichot D Nimkulrat, Julia Lemanski, Nicolas G Pintozzi, Valentina Lo Sardo, Barak Blum

bioRxiv : the preprint server for biology. 2026 March 27.
The RNA-binding protein CPEB1 marks healthy adult β cells in mice but is dispensable for β cell identity and function

Sutichot D Nimkulrat, Matthew R Wagner, Bayley J Waters, Nicolas G Pintozzi, Maria Del Carmen Mendoza Niemes, Cyrus R Sethna, Hariharan Jayaraaman, Barak Blum

Scientific reports. 2025 December 13.
Kidney deletions of Cyp27b1 fail to reduce serum 1,25(OH)<sub>2</sub>D<sub>3</sub>

Seong Min Lee, Shannon R Cichanski, Nicolas G Pintozzi, Martin Kaufmann, Glenville Jones, Mark B Meyer

The Journal of steroid biochemistry and molecular biology. 2025 March 17.
TIFAB modulates metabolic pathways in KMT2A::MLLT3-induced AML through HNF4A

Yang Wang, Yan Xiu, Qianze Dong, Jinming Zhao, Kelao Neumbo, Masaru Miyagi, Nicholas Borcherding, Lin Fu, Havana De Celis, Nicolas Pintozzi, Daniel T Starczynowski, Chen Zhao

Blood advances. 2024 December 3.

The risk of developing type 2 diabetes (T2D) has increased five percent yearly over the past decade, yet young adults with Down syndrome have a ten-fold higher probability. Although elevated BMI at younger ages may contribute to this increased risk for T2D, the trisomy of Dyrk1a and Rcan1 on chromosome 21, previously shown to decrease beta cell proliferation when overexpressed, represents a novel genetic explanation. We hypothesize that genetically stunted beta cell proliferation during metabolic stress increases the risk of T2D for individuals with Down syndrome. Utilizing the Ts65Dn mouse model of Down syndrome, I aim to distinguish the rate of pancreatic islet proliferation during metabolic stress and determine why it differs from wild-type mice.