Publications

Sue Menko, PhD

Contact

Name: Sue Menko, PhD
Position: Professor

1020 Locust Street
Jefferson Alumni Hall, Room 564
Philadelphia, PA 19107

Telephone: 215-503-2166

Highlighted Publications

Basu, S, Rajakaruna, S, and Menko, AS (2012) Insulin-like growth factor receptor-1 and nuclear factor kappa B are crucial survival signals that regulate caspase-3 mediated lens epithelial cell differentiation initiation J Biol Chem. 287(11):8384-97. Epub 2012 Jan 24. PMID:22275359 PMCID:PMC3381865

This study reveals an IGF-1R signaling pathway that is a crucial regulator of caspase-3 activation, responsible for maintaining caspase-3 at the low level at which it functions in the initiation of lens epithelial cell differentiation.  

Menko AS, Bleaken BM, Libowitz AA, Zhang L, Stepp MA, Walker JL (2014) A central role for vimentin in regulating repair function during healing of the lens epithelium. Mol Biol Cell. 25(6):776-90. Epub 2014 Jan 29. PMID:24478454 PMCID:PMC3952848

This study shows that the lens contains a resident mesenchymal cell population that directs regenerative repair of the lens epithelium, post-cataract surgery, in a mechanism that is dependent on the function of the cytoskeletal protein vimentin.

Logan CM, Bowen, CJ, Menko AS (2017) Induction of immune surveillance of the dysmorphogenic lens. Sci Rep 7(1):16235. PMID:29176738 PMCID: PMC5701161

In this study with our lens-specific N-cadherin knockout mice, we discovered that the lens, previously considered immune privileged, is instead immune quiescent. Immune cells are recruited to these dysgenic lenses, likely migrating across LYVE-1-rich ciliary zonules, and are induced to become myofibroblasts associated with lens opacity.

Recent Publications

BNIP3L/NIX is required for elimination of mitochondria, endoplasmic reticulum and Golgi apparatus during eye lens organelle-free zone formation

In wound repair vimentin mediates the transition of mesenchymal leader cells to a myofibroblast phenotype

Induction of immune surveillance of the dysmorphogenic lens

N-cadherin regulates signaling mechanisms required for lens fiber cell elongation and lens morphogenesis

New insight into the protrusions and paddles that link lens fiber cells

Cells activated for wound repair have the potential to direct collective invasion of an epithelium

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Establishment of a clinically relevant ex vivo mock cataract surgery model for investigating epithelial wound repair in a native microenvironment

Endogenous hydrogen peroxide production in the epithelium of the developing embryonic lens

A central role for vimentin in regulating repair function during healing of the lens epithelium

Regional-specific alterations in cell-cell junctions, cytoskeletal networks and myosin-mediated mechanical cues coordinate collectivity of movement of epithelial cells in response to injury

α6 integrin transactivates insulin-like growth factor receptor-1 (IGF-1R) to regulate caspase-3-mediated lens epithelial cell differentiation initiation

Suppression of MAPK/JNK-MTORC1 signaling leads to premature loss of organelles and nuclei by autophagy during terminal differentiation of lens fiber cells

Differentiation state-specific mitochondrial dynamic regulatory networks are revealed by global transcriptional analysis of the developing chicken lens

Autophagy and mitophagy participate in ocular lens organelle degradation

The hippo signaling pathway is required for salivary gland development and its dysregulation is associated with sjogren's syndrome

Distinct roles for N-Cadherin linked c-Src and fyn kinases in lens development

Insulin-like growth factor receptor-1 and nuclear factor κB are crucial survival signals that regulate caspase-3-mediated lens epithelial cell differentiation initiation

Modulation of N-cadherin junctions and their role as epicenters of differentiation-specific actin regulation in the developing lens

Unique precursors for the mesenchymal cells involved in injury response and fibrosis

Erratum: Mechanism of small heat shock protein function in vivo. A knock-in mouse model demonstrates that the R49C mutation in αA-crystallin enhances protein insolubility and cell death (The Journal of Biological Chemistry (2008) vol. 283 (5801-5814) 10.1074/ A708704200)

Noggin producing, MyoD-positive cells are crucial for eye development

Overexpression of DPAGT1 leads to aberrant N-glycosylation of E-cadherin and cellular discohesion in oral cancer

Integrins in lens development and disease

Diverse roles of E-cadherin in the morphogenesis of the submandibular gland: Insights into the formation of acinar and ductal structures