Faculty Appointments
Assistant Professor of Medicine
Assistant Professor of Biomedical EngineeringAssistant Professor of Biochemistry
Education
Ph.D., Chemical Biology, Harvard University, Cambridge, MassachusettsB.A., Biochemistry, University of Pennsylvania, Philadelphia, PennsylvaniaM.S., Chemistry, University of Pennsylvania, Philadelphia, Pennsylvania
Research Description
The overarching focus of my research laboratory is understanding the role of the extracellular matrix (ECM) in musculoskeletal biology, particularly of carbohydrate-mediated signaling and differentiation as regulated by glycosaminoglycans (GAGs). Glycosaminoglycans are unbranched polysaccharides that are abundantly present in many organ systems in the body. In musculoskeletal tissues, GAGs are typically thought to serve primarily structural roles, as they are highly polar, hydrophilic moieties capable of high osmotic swelling pressure. However, there is mounting evidence that GAGs in the ECM interact with secreted signaling molecules, cells, and other ECM components, and these interactions play a substantial role in controlling the activity of resident cells and subsequent tissue development, function, and homeostasis. While the primary molecules of interest are GAGs, our research encompasses the investigation of related ECM components such as collagens and growth factors that interact with GAGs to carry out important biological functions. We combine analytical chemistry, biochemistry, and molecular biology methods to identify the chemical composition of the ECM and how particular components regulate development and homeostasis, as well as how dysregulated ECM deposition or degradation contribute to disease or degeneration. Ultimately, we seek to understand these mechanisms in order to develop regenerative therapies for bone, intervertebral disc, and cartilage. To this end, we have multiple ongoing projects in the lab that are designed to elucidate normal and pathologic contributions of the ECM in musculoskeletal tissues.
1. Dysregulated extracellular matrix deposition in heterotopic ossification.
- Heterotopic ossification (HO) is the pathologic formation of bone in extra-skeletal tissues. HO can develop following significant trauma such as blast, brain, or spinal cord injuries, burns, or after routine surgical procedures such as joint replacement or amputation surgery. Ectopic bone formation leads to impaired wound healing, chronic infection, and chronic pain, which can hinder mobility and function as well as the use of prosthetics. This can lead to further related health complications such as opioid addiction, depression, and suicide. HO affects the Veteran population disproportionately but has been found in all patient populations. The molecular mechanisms that drive this aberrant bone formation are not well-understood, and thus, effective therapeutics are lacking. We are focused on elucidating the mechanisms underlying aberrant bone formation as driven by tissue and molecular level changes to the ECM.
2. Extracellular matrix-mediated signaling and patterning in early spine development.
- The embryonic notochord is a unique, transient structure that serves as the main signaling center for directing developmental patterning. The notochord starts out as a GAG-rich rod-like structure, which over time becomes sequestered in the ECM-rich central region of the intervertebral disc referred to as the nucleus pulposus (NP). My previous work identified large changes in global expression profiles of ECM molecules during this notochord to NP transition. However, the molecular details of how this GAG-rich structure directs spine patterning and transforms into the NP in early embryonic development remains unknown. We are interested in identifying ECM-mediated signaling that drive spine formation.
3. Extracellular matrix regeneration as a therapeutic strategy for back pain.
- The nucleus pulposus (NP) is the ECM-rich central region of the intervertebral disc that is responsible for distributing compressive loads on the spine. Pathological changes to this region are often thought to initiate progressive structural deterioration of the entire intervertebral joint. Degeneration of the disc is strongly implicated as a cause of low back pain, which ~85% of people will experience in their lifetime. This is a significant clinical problem that results in over $100 billion in healthcare and socioeconomic costs every year. Current treatments are mostly palliative, and the fraction of patients who are candidates for surgical interventions have high failure rates. Importantly, none of the available treatments maintain or restore native disc structure or biomechanical function, and thus, there is a significant clinical need to develop therapeutic approaches that manage symptoms as well as regenerate native disc tissue. We are working to elucidate the pathologic breakdown of the ECM that leads to intervertebral disc degeneration on the molecular level. Furthermore, in conjunction with our interests in identifying the ECM-mediated signaling that drives early NP formation, we are working on applying these developmental signals to induce ECM formation as a potential treatment option for disc degeneration.
4. Pathological changes to extracellular matrix composition as a result of sepsis.
- Systemic inflammatory response syndrome, or sepsis, is a serious medical condition with a high mortality rate. Even following recovery, sepsis patients often suffer from a myriad of long-lasting medical complications, which include neurological dysfunction, cardiovascular disease, and musculoskeletal disability. Interestingly, the organ systems that are affected in post-sepsis syndrome are often not the site of the primary infection that leads to sepsis. In collaboration with Dr. Fiona Harrison (Division of Diabetes and Endocrinology and The Vanderbilt Brain Institute), we are seeking to understand the molecular connections between systemic inflammation and resulting secondary pathology by elucidating the changes that occur in ECM metabolism as a result of sepsis.
Other areas of interest in development:
1. The role of extracellular matrix synthesis in bone formation and fracture healing.
2. The effects of metabolic disorders (obesity, diabetes, etc.) on extracellular matrix synthesis in wound healing.
1. Dysregulated extracellular matrix deposition in heterotopic ossification.
- Heterotopic ossification (HO) is the pathologic formation of bone in extra-skeletal tissues. HO can develop following significant trauma such as blast, brain, or spinal cord injuries, burns, or after routine surgical procedures such as joint replacement or amputation surgery. Ectopic bone formation leads to impaired wound healing, chronic infection, and chronic pain, which can hinder mobility and function as well as the use of prosthetics. This can lead to further related health complications such as opioid addiction, depression, and suicide. HO affects the Veteran population disproportionately but has been found in all patient populations. The molecular mechanisms that drive this aberrant bone formation are not well-understood, and thus, effective therapeutics are lacking. We are focused on elucidating the mechanisms underlying aberrant bone formation as driven by tissue and molecular level changes to the ECM.
2. Extracellular matrix-mediated signaling and patterning in early spine development.
- The embryonic notochord is a unique, transient structure that serves as the main signaling center for directing developmental patterning. The notochord starts out as a GAG-rich rod-like structure, which over time becomes sequestered in the ECM-rich central region of the intervertebral disc referred to as the nucleus pulposus (NP). My previous work identified large changes in global expression profiles of ECM molecules during this notochord to NP transition. However, the molecular details of how this GAG-rich structure directs spine patterning and transforms into the NP in early embryonic development remains unknown. We are interested in identifying ECM-mediated signaling that drive spine formation.
3. Extracellular matrix regeneration as a therapeutic strategy for back pain.
- The nucleus pulposus (NP) is the ECM-rich central region of the intervertebral disc that is responsible for distributing compressive loads on the spine. Pathological changes to this region are often thought to initiate progressive structural deterioration of the entire intervertebral joint. Degeneration of the disc is strongly implicated as a cause of low back pain, which ~85% of people will experience in their lifetime. This is a significant clinical problem that results in over $100 billion in healthcare and socioeconomic costs every year. Current treatments are mostly palliative, and the fraction of patients who are candidates for surgical interventions have high failure rates. Importantly, none of the available treatments maintain or restore native disc structure or biomechanical function, and thus, there is a significant clinical need to develop therapeutic approaches that manage symptoms as well as regenerate native disc tissue. We are working to elucidate the pathologic breakdown of the ECM that leads to intervertebral disc degeneration on the molecular level. Furthermore, in conjunction with our interests in identifying the ECM-mediated signaling that drives early NP formation, we are working on applying these developmental signals to induce ECM formation as a potential treatment option for disc degeneration.
4. Pathological changes to extracellular matrix composition as a result of sepsis.
- Systemic inflammatory response syndrome, or sepsis, is a serious medical condition with a high mortality rate. Even following recovery, sepsis patients often suffer from a myriad of long-lasting medical complications, which include neurological dysfunction, cardiovascular disease, and musculoskeletal disability. Interestingly, the organ systems that are affected in post-sepsis syndrome are often not the site of the primary infection that leads to sepsis. In collaboration with Dr. Fiona Harrison (Division of Diabetes and Endocrinology and The Vanderbilt Brain Institute), we are seeking to understand the molecular connections between systemic inflammation and resulting secondary pathology by elucidating the changes that occur in ECM metabolism as a result of sepsis.
Other areas of interest in development:
1. The role of extracellular matrix synthesis in bone formation and fracture healing.
2. The effects of metabolic disorders (obesity, diabetes, etc.) on extracellular matrix synthesis in wound healing.
Research Keywords
Musculoskeletal biology, extracellular matrix, glycosaminoglycans, bone, spine, intervertebral disc, sepsis, neurodegeneration, healing, regenerative therapies
Publications
Petronglo JR, Putnam NE, Ford CA, Cruz-Victorio V, Curry JM, Butrico CE, Fulbright LE, Johnson JR, Peck SH, Fatah SR, Cassat JE. Context-Dependent Roles for Toll-Like Receptors 2 and 9 in the Pathogenesis of Staphylococcus aureus Osteomyelitis. Infect Immun [print-electronic]. 2022 Oct 10/13/2022; e0041722. PMID: 36226943, DOI: 10.1128/iai.00417-22, ISSN: 1098-5522.
Lau YK, Peck SH, Arginteanu T, Wu M, Lin M, Shore EM, Klein PS, Casal ML, Smith LJ. Effects of lithium administration on vertebral bone disease in mucopolysaccharidosis I dogs. Bone [print-electronic]. 2022 Jan; 154: 116237. PMID: 34695616, PMCID: PMC8671266, PII: S8756-3282(21)00403-8, DOI: 10.1016/j.bone.2021.116237, ISSN: 1873-2763.
Hickman TT, Rathan-Kumar S, Peck SH. Development, Pathogenesis, and Regeneration of the Intervertebral Disc: Current and Future Insights Spanning Traditional to Omics Methods. Front Cell Dev Biol. 2022; 10: 841831. PMID: 35359439, PMCID: PMC8963184, PII: 841831, DOI: 10.3389/fcell.2022.841831, ISSN: 2296-634X.
Ford CA, Hurford IM, Fulbright LE, Curry JM, Peek CT, Spoonmore TJ, Cruz Victorio V, Johnson JR, Peck SH, Cassat JE. Loss of Vhl alters trabecular bone loss during S. aureus osteomyelitis in a cell-specific manner. Front Cell Infect Microbiol. 2022; 12: 985467. PMID: 36204648, PMCID: PMC9530664, DOI: 10.3389/fcimb.2022.985467, ISSN: 2235-2988.
Peck SH, Lau YK, Kang JL, Lin M, Arginteanu T, Matalon DR, Bendigo JR, O'Donnell P, Haskins ME, Casal ML, Smith LJ. Progression of vertebral bone disease in mucopolysaccharidosis VII dogs from birth to skeletal maturity. Mol Genet Metab [print-electronic]. 2021 Aug; 133(4): 378-85. PMID: 34154922, PMCID: PMC8289741, PII: S1096-7192(21)00732-0, DOI: 10.1016/j.ymgme.2021.06.005, ISSN: 1096-7206.
Boller LA, Shiels SM, Florian DC, Peck SH, Schoenecker JG, Duvall C, Wenke JC, Guelcher SA. Effects of nanocrystalline hydroxyapatite concentration and skeletal site on bone and cartilage formation in rats. Acta Biomater [print-electronic]. 2021 Aug; 130: 485-96. PMID: 34129957, PII: S1742-7061(21)00366-4, DOI: 10.1016/j.actbio.2021.05.056, ISSN: 1878-7568.
Boller LA, Shiels SM, Florian DC, Peck SH, Schoenecker JG, Duvall C, Wenke JC, Guelcher SA. Effects of nanocrystalline hydroxyapatite concentration and skeletal site on bone and cartilage formation in rats. Acta Biomater [print-electronic]. 2021 Aug; 130: 485-96. PMID: 34129957, PMCID: PMC9169158, PII: S1742-7061(21)00366-4, DOI: 10.1016/j.actbio.2021.05.056, ISSN: 1878-7568.
Towler OW, Peck SH, Kaplan FS, Shore EM. Dysregulated BMP signaling through ACVR1 impairs digit joint development in fibrodysplasia ossificans progressiva (FOP). Dev Biol [print-electronic]. 2021 Feb; 470: 136-46. PMID: 33217406, PMCID: PMC8035973, PII: S0012-1606(20)30296-7, DOI: 10.1016/j.ydbio.2020.11.004, ISSN: 1095-564X.
Peck SH, Tobias JW, Shore EM, Malhotra NR, Haskins ME, Casal ML, Smith LJ. Molecular profiling of failed endochondral ossification in mucopolysaccharidosis VII. Bone [print-electronic]. 2019 Nov; 128: 115042. PMID: 31442675, PMCID: PMC6813906, PII: S8756-3282(19)30330-8, DOI: 10.1016/j.bone.2019.115042, ISSN: 1873-2763.
Peck SH, Bendigo JR, Tobias JW, Dodge GR, Malhotra NR, Mauck RL, Smith LJ. Hypoxic Preconditioning Enhances Bone Marrow-Derived Mesenchymal Stem Cell Survival in a Low Oxygen and Nutrient-Limited 3D Microenvironment. Cartilage [print-electronic]. 2019 Apr 4/11/2019; 1947603519841675. PMID: 30971109, DOI: 10.1177/1947603519841675, ISSN: 1947-6043.
Adhikari B, De Silva B, Molina JA, Allen A, Peck SH, Lee SY. Neuronal ceroid lipofuscinosis related ER membrane protein CLN8 regulates PP2A activity and ceramide levels. Biochim Biophys Acta Mol Basis Dis [print-electronic]. 2019 Feb 2/1/2019; 1865(2): 322-8. PMID: 30453012, PII: S0925-4439(18)30472-1, DOI: 10.1016/j.bbadis.2018.11.011, ISSN: 1879-260X.
Piazza M, Peck SH, Gullbrand SE, Bendigo JR, Arginteanu T, Zhang Y, Smith HE, Malhotra NR, Smith LJ. Quantitative MRI correlates with histological grade in a percutaneous needle injury mouse model of disc degeneration. J. Orthop. Res [print-electronic]. 2018 Oct; 36(10): 2771-9. PMID: 29687490, PMCID: PMC6200662, DOI: 10.1002/jor.24028, ISSN: 1554-527X.
Riester SM, Lin Y, Wang W, Cong L, Mohamed Ali AM, Peck SH, Smith LJ, Currier BL, Clark M, Huddleston P, Krauss W, Yaszemski MJ, Morrey ME, Abdel MP, Bydon M, Qu W, Larson AN, van Wijnen AJ, Nassr A. RNA sequencing identifies gene regulatory networks controlling extracellular matrix synthesis in intervertebral disk tissues. J. Orthop. Res [print-electronic]. 2018 May; 36(5): 1356-69. PMID: 29227558, PMCID: PMC5990467, DOI: 10.1002/jor.23834, ISSN: 1554-527X.
Peck SH, McKee KK, Tobias JW, Malhotra NR, Harfe BD, Smith LJ. Whole Transcriptome Analysis of Notochord-Derived Cells during Embryonic Formation of the Nucleus Pulposus. Sci Rep. 2017 Sep 9/5/2017; 7(1): 10504. PMID: 28874804, PMCID: PMC5585380, PII: 10.1038/s41598-017-10692-5, DOI: 10.1038/s41598-017-10692-5, ISSN: 2045-2322.
Peck SH, Casal ML, Malhotra NR, Ficicioglu C, Smith LJ. Pathogenesis and treatment of spine disease in the mucopolysaccharidoses. Mol. Genet. Metab [print-electronic]. 2016 Aug; 118(4): 232-43. PMID: 27296532, PMCID: PMC4970936, PII: S1096-7192(16)30095-6, DOI: 10.1016/j.ymgme.2016.06.002, ISSN: 1096-7206.
Peck SH, O'Donnell PJ, Kang JL, Malhotra NR, Dodge GR, Pacifici M, Shore EM, Haskins ME, Smith LJ. Delayed hypertrophic differentiation of epiphyseal chondrocytes contributes to failed secondary ossification in mucopolysaccharidosis VII dogs. Mol. Genet. Metab [print-electronic]. 2015 Nov; 116(3): 195-203. PMID: 26422116, PMCID: PMC4641049, PII: S1096-7192(15)30054-8, DOI: 10.1016/j.ymgme.2015.09.008, ISSN: 1096-7206.
Moharir A, Peck SH, Budden T, Lee SY. The role of N-glycosylation in folding, trafficking, and functionality of lysosomal protein CLN5. PLoS ONE. 2013; 8(9): e74299. PMID: 24058541, PMCID: PMC3769244, PII: PONE-D-13-08979, DOI: 10.1371/journal.pone.0074299, ISSN: 1932-6203.
Peck SH, Chen I, Liu DR. Directed evolution of a small-molecule-triggered intein with improved splicing properties in mammalian cells. Chem. Biol. 2011 May 5/27/2011; 18(5): 619-30. PMID: 21609843, PMCID: PMC3124510, PII: S1074-5521(11)00122-0, DOI: 10.1016/j.chembiol.2011.02.014, ISSN: 1879-1301.
Karanicolas J, Corn JE, Chen I, Joachimiak LA, Dym O, Peck SH, Albeck S, Unger T, Hu W, Liu G, Delbecq S, Montelione GT, Spiegel CP, Liu DR, Baker D. A de novo protein binding pair by computational design and directed evolution. Mol. Cell [print-electronic]. 2011 Apr 4/22/2011; 42(2): 250-60. PMID: 21458342, PMCID: PMC3102007, PII: S1097-2765(11)00208-5, DOI: 10.1016/j.molcel.2011.03.010, ISSN: 1097-4164.
Lau YK, Peck SH, Arginteanu T, Wu M, Lin M, Shore EM, Klein PS, Casal ML, Smith LJ. Effects of lithium administration on vertebral bone disease in mucopolysaccharidosis I dogs. Bone [print-electronic]. 2022 Jan; 154: 116237. PMID: 34695616, PMCID: PMC8671266, PII: S8756-3282(21)00403-8, DOI: 10.1016/j.bone.2021.116237, ISSN: 1873-2763.
Hickman TT, Rathan-Kumar S, Peck SH. Development, Pathogenesis, and Regeneration of the Intervertebral Disc: Current and Future Insights Spanning Traditional to Omics Methods. Front Cell Dev Biol. 2022; 10: 841831. PMID: 35359439, PMCID: PMC8963184, PII: 841831, DOI: 10.3389/fcell.2022.841831, ISSN: 2296-634X.
Ford CA, Hurford IM, Fulbright LE, Curry JM, Peek CT, Spoonmore TJ, Cruz Victorio V, Johnson JR, Peck SH, Cassat JE. Loss of Vhl alters trabecular bone loss during S. aureus osteomyelitis in a cell-specific manner. Front Cell Infect Microbiol. 2022; 12: 985467. PMID: 36204648, PMCID: PMC9530664, DOI: 10.3389/fcimb.2022.985467, ISSN: 2235-2988.
Peck SH, Lau YK, Kang JL, Lin M, Arginteanu T, Matalon DR, Bendigo JR, O'Donnell P, Haskins ME, Casal ML, Smith LJ. Progression of vertebral bone disease in mucopolysaccharidosis VII dogs from birth to skeletal maturity. Mol Genet Metab [print-electronic]. 2021 Aug; 133(4): 378-85. PMID: 34154922, PMCID: PMC8289741, PII: S1096-7192(21)00732-0, DOI: 10.1016/j.ymgme.2021.06.005, ISSN: 1096-7206.
Boller LA, Shiels SM, Florian DC, Peck SH, Schoenecker JG, Duvall C, Wenke JC, Guelcher SA. Effects of nanocrystalline hydroxyapatite concentration and skeletal site on bone and cartilage formation in rats. Acta Biomater [print-electronic]. 2021 Aug; 130: 485-96. PMID: 34129957, PII: S1742-7061(21)00366-4, DOI: 10.1016/j.actbio.2021.05.056, ISSN: 1878-7568.
Boller LA, Shiels SM, Florian DC, Peck SH, Schoenecker JG, Duvall C, Wenke JC, Guelcher SA. Effects of nanocrystalline hydroxyapatite concentration and skeletal site on bone and cartilage formation in rats. Acta Biomater [print-electronic]. 2021 Aug; 130: 485-96. PMID: 34129957, PMCID: PMC9169158, PII: S1742-7061(21)00366-4, DOI: 10.1016/j.actbio.2021.05.056, ISSN: 1878-7568.
Towler OW, Peck SH, Kaplan FS, Shore EM. Dysregulated BMP signaling through ACVR1 impairs digit joint development in fibrodysplasia ossificans progressiva (FOP). Dev Biol [print-electronic]. 2021 Feb; 470: 136-46. PMID: 33217406, PMCID: PMC8035973, PII: S0012-1606(20)30296-7, DOI: 10.1016/j.ydbio.2020.11.004, ISSN: 1095-564X.
Peck SH, Tobias JW, Shore EM, Malhotra NR, Haskins ME, Casal ML, Smith LJ. Molecular profiling of failed endochondral ossification in mucopolysaccharidosis VII. Bone [print-electronic]. 2019 Nov; 128: 115042. PMID: 31442675, PMCID: PMC6813906, PII: S8756-3282(19)30330-8, DOI: 10.1016/j.bone.2019.115042, ISSN: 1873-2763.
Peck SH, Bendigo JR, Tobias JW, Dodge GR, Malhotra NR, Mauck RL, Smith LJ. Hypoxic Preconditioning Enhances Bone Marrow-Derived Mesenchymal Stem Cell Survival in a Low Oxygen and Nutrient-Limited 3D Microenvironment. Cartilage [print-electronic]. 2019 Apr 4/11/2019; 1947603519841675. PMID: 30971109, DOI: 10.1177/1947603519841675, ISSN: 1947-6043.
Adhikari B, De Silva B, Molina JA, Allen A, Peck SH, Lee SY. Neuronal ceroid lipofuscinosis related ER membrane protein CLN8 regulates PP2A activity and ceramide levels. Biochim Biophys Acta Mol Basis Dis [print-electronic]. 2019 Feb 2/1/2019; 1865(2): 322-8. PMID: 30453012, PII: S0925-4439(18)30472-1, DOI: 10.1016/j.bbadis.2018.11.011, ISSN: 1879-260X.
Piazza M, Peck SH, Gullbrand SE, Bendigo JR, Arginteanu T, Zhang Y, Smith HE, Malhotra NR, Smith LJ. Quantitative MRI correlates with histological grade in a percutaneous needle injury mouse model of disc degeneration. J. Orthop. Res [print-electronic]. 2018 Oct; 36(10): 2771-9. PMID: 29687490, PMCID: PMC6200662, DOI: 10.1002/jor.24028, ISSN: 1554-527X.
Riester SM, Lin Y, Wang W, Cong L, Mohamed Ali AM, Peck SH, Smith LJ, Currier BL, Clark M, Huddleston P, Krauss W, Yaszemski MJ, Morrey ME, Abdel MP, Bydon M, Qu W, Larson AN, van Wijnen AJ, Nassr A. RNA sequencing identifies gene regulatory networks controlling extracellular matrix synthesis in intervertebral disk tissues. J. Orthop. Res [print-electronic]. 2018 May; 36(5): 1356-69. PMID: 29227558, PMCID: PMC5990467, DOI: 10.1002/jor.23834, ISSN: 1554-527X.
Peck SH, McKee KK, Tobias JW, Malhotra NR, Harfe BD, Smith LJ. Whole Transcriptome Analysis of Notochord-Derived Cells during Embryonic Formation of the Nucleus Pulposus. Sci Rep. 2017 Sep 9/5/2017; 7(1): 10504. PMID: 28874804, PMCID: PMC5585380, PII: 10.1038/s41598-017-10692-5, DOI: 10.1038/s41598-017-10692-5, ISSN: 2045-2322.
Peck SH, Casal ML, Malhotra NR, Ficicioglu C, Smith LJ. Pathogenesis and treatment of spine disease in the mucopolysaccharidoses. Mol. Genet. Metab [print-electronic]. 2016 Aug; 118(4): 232-43. PMID: 27296532, PMCID: PMC4970936, PII: S1096-7192(16)30095-6, DOI: 10.1016/j.ymgme.2016.06.002, ISSN: 1096-7206.
Peck SH, O'Donnell PJ, Kang JL, Malhotra NR, Dodge GR, Pacifici M, Shore EM, Haskins ME, Smith LJ. Delayed hypertrophic differentiation of epiphyseal chondrocytes contributes to failed secondary ossification in mucopolysaccharidosis VII dogs. Mol. Genet. Metab [print-electronic]. 2015 Nov; 116(3): 195-203. PMID: 26422116, PMCID: PMC4641049, PII: S1096-7192(15)30054-8, DOI: 10.1016/j.ymgme.2015.09.008, ISSN: 1096-7206.
Moharir A, Peck SH, Budden T, Lee SY. The role of N-glycosylation in folding, trafficking, and functionality of lysosomal protein CLN5. PLoS ONE. 2013; 8(9): e74299. PMID: 24058541, PMCID: PMC3769244, PII: PONE-D-13-08979, DOI: 10.1371/journal.pone.0074299, ISSN: 1932-6203.
Peck SH, Chen I, Liu DR. Directed evolution of a small-molecule-triggered intein with improved splicing properties in mammalian cells. Chem. Biol. 2011 May 5/27/2011; 18(5): 619-30. PMID: 21609843, PMCID: PMC3124510, PII: S1074-5521(11)00122-0, DOI: 10.1016/j.chembiol.2011.02.014, ISSN: 1879-1301.
Karanicolas J, Corn JE, Chen I, Joachimiak LA, Dym O, Peck SH, Albeck S, Unger T, Hu W, Liu G, Delbecq S, Montelione GT, Spiegel CP, Liu DR, Baker D. A de novo protein binding pair by computational design and directed evolution. Mol. Cell [print-electronic]. 2011 Apr 4/22/2011; 42(2): 250-60. PMID: 21458342, PMCID: PMC3102007, PII: S1097-2765(11)00208-5, DOI: 10.1016/j.molcel.2011.03.010, ISSN: 1097-4164.