Author

L. Haataja

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 6 Biochemistry· 1 Pathology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 7 Research Focus:cell type annotation· 5 Organism:human· 5 Assay:proteomics· 4 Research Focus:differential expression· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 2

Frequent Co-Authors

P. Arvan· 8 shared A. Arunagiri· 2 shared B. Dhayalan· 2 shared D. Larkin· 2 shared F. Barbetti· 2 shared L. Sui· 2 shared M. A. Weiss· 2 shared M. Liu· 2 shared

Activity by Year

2019-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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8 shared papersCell Biology

P. Arvan

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8 papers

Recent·Most cited

Permanent Neonatal diabetes-causing Insulin mutations have dominant negative effects on beta cell identity

Y. Zhang, L. Sui, Q. Du, L. Haataja, Y. Yin, R. Viola, S. Xu, C. U. Nielsson, R. L. Leibel, F. Barbetti, P. Arvan, D. Egli

This study investigates two INS mutations causing permanent neonatal diabetes, showing they impair beta cell function through misfolded proinsulin, ER stress, and dedifferentiation.

bioRxiv · Sep 1, 2023Cell Biology

Retrograde mitochondrial signaling governs the identity and maturity of metabolic tissues

G. L. Pearson, E. M. Walker, N. Lawlor, A. Lietzke, V. Sidarala, J. Zhu, T. Stromer, E. C. Reck, A. M. Stendahl, J. Li, E. Levi-D'Ancona, M. B. Pasmooij, D. L. Hubers, A. Renberg, K. Mohamed, , S. A. Soleimanpour

This study shows that mitochondrial dysfunction triggers a retrograde signaling program that reduces cellular maturity in metabolic tissues, and blocking this signaling can restore cell identity and improve hyperglycemia.

bioRxiv · Aug 2, 2022 · PreprintCell Biology

Predisposition to Proinsulin Misfolding as a Genetic Risk to Diet-Induced Diabetes

M. Alam, A. Arunagiri, L. Haataja, M. Torres, D. Larkin, J. Kappler, N. Jin, P. Arvan

This study shows that a proinsulin mutation increases susceptibility to diet-induced diabetes in mice, with severity linked to genetic dosage and beta-cell dysfunction.

bioRxiv · Jun 1, 2021Cell Biology

Distinct states of proinsulin misfolding in MIDY

L. Haataja, A. Arunagiri, A. Hassan, K. Regan, B. Tsai, B. Dhayalan, M. A. Weiss, M. Liu, P. Arvan

The paper investigates proinsulin misfolding in MIDY mutants, showing that disrupting the Cys(A6)-Cys(A11) bond can restore proper folding and ER export in some mutants.

bioRxiv · May 10, 2021Biochemistry

The type 2 diabetes gene product STARD10 is a phosphoinositide binding protein that controls insulin secretory granule biogenesis

G. R. Carrat, E. Haythorne, A. Tomas, L. Haataja, A. Mueller, P. Arvan, A. Piunti, K. Cheng, M. Huang, T. Pullen, E. Georgiadou, T. Stylianides, N. S. Amirruddin, V. Salem, W. Distaso, , G. A. Rutter

This study identifies STARD10 as a phosphoinositide binding protein that regulates insulin granule biogenesis in beta-cells by affecting phosphatidylinositol levels and proinsulin processing.

Molecular Metabolism · Oct 1, 2020Peer-reviewedCell Biology

Establishing cell-intrinsic limitations in cell cycle progression controls graft growth and promotes differentiation of pancreatic endocrine cells

L. Sui, D. M. Egli, Y. Xin, D. C. Georgieva, G. Diedenhofen, L. Haataja, Q. Su, Y. Wang, M. Zuccaro, J. Kim, J. Fu, Y. Xing, D. Baum, P. Arvan, F. Barbetti, , R. Goland

The paper investigates how limitations in S-phase progression affect pancreatic endocrine differentiation and graft growth, finding that impaired DNA replication enhances differentiation and prevents cystic growth.

bioRxiv · Mar 13, 2020Cell Biology

Role of Proinsulin Self-Association in Mutant INS gene-induced Diabetes of Youth

M. Liu, P. Arvan, J. Sun, Y. Xiong, X. Li, L. Haataja, W. Chen, S. A. Mir, R. Madley, D. Larkin, A. Anjum, B. Dhayalan, N. K. Rege, N. D. Wickramasinghe, M. A. Weiss, , D. A. Ostrov

This study identifies proinsulin self-association as a mechanism driving dominant-negative effects of misfolded proinsulin in MIDY, offering a therapeutic target for enhancing insulin production.

bioRxiv · Oct 1, 2019Cell Biology

Abnormalities in Proinsulin Processing in Islets from Individuals with Longstanding T1D

E. K. Sims, J. Nyalwidhe, F. Syed, H. T. Bahnson, L. Haataja, C. Speake, M. Morris, R. G. Mirmira, J. Nadler, T. L. Mastracci, P. Arvan, C. J. Greenbaum, C. Evans-Molina

The paper investigates proinsulin processing abnormalities in T1D islets, finding reduced processing enzymes and cytokine-induced expression changes.

bioRxiv · Feb 8, 2019Pathology