Author

L. L. Wallrath

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

Biology Disciplines

Click to filter author papers

Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Organism:human· 1

Frequent Co-Authors

J. Lammerding· 2 shared T. J. Kirby· 2 shared A. J. Earle· 1 shared A. M. Gacita· 1 shared C. D. Morsink· 1 shared C. S. Stipp· 1 shared E. McNally· 1 shared G. Bonne· 1 shared

Activity by Year

2019-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCell Biology

J. Lammerding

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The 4T1 breast carcinoma model possesses hybrid epithelial/mesenchymal traits linked to a highly metastatic phenotype

M. E. Herndon, K. Gibson-Corley, L. L. Wallrath, M. Henry, C. S. Stipp

This study investigates E-cadherin's role in 4T1 breast carcinoma metastasis, finding that E-cadherin is retained and does not determine metastatic capacity, with cells displaying hybrid epithelial/mesenchymal traits.

bioRxiv · Feb 2, 2024 · PreprintCancer Biology

Nuclear damage in LMNA mutant iPSC-derived cardiomyocytes is associated with impaired lamin localization to the nuclear envelope

M. Wallace, H. Zahr, S. Perati, C. D. Morsink, L. E. Johnson, A. M. Gacita, S. Lai, L. L. Wallrath, I. J. Benjamin, E. McNally, T. J. Kirby, J. Lammerding

This study shows that LMNA mutations in iPSC-derived cardiomyocytes cause nuclear shape changes, reduced stiffness, and lamin mislocalization, linking nuclear abnormalities to LMNA-DCM pathogenesis.

bioRxiv · Oct 30, 2021 · PreprintCell Biology

Mutant lamins cause nuclear envelope rupture and DNA damage in skeletal muscle cells

A. J. Earle, T. J. Kirby, G. R. Fedorchak, P. Isermann, J. Patel, S. Iruvanti, S. A. Moore, G. Bonne, L. L. Wallrath, J. Lammerding

This study shows that LMNA mutations cause nuclear envelope rupture and DNA damage in muscle cells, leading to disease through mechanical stress and DNA damage pathways.

bioRxiv · Aug 17, 2019Cell Biology