Loma Linda University

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Kerby Oberg, MD, PhD
Professor, Pathology and Human Anatomy
School of Medicine
Member, Anatomy, SM, Faculty of Graduate Studies
Publications    Book Review - Scholarly Journals--Published
  • Oberg, KC. 2009. Review of “Freaks of Nature: What Anomalies Tell Us About Development and Evolution”. Doody''s Review Service (on-line). Available:http://www.doody.com ( 5/2009 )
  Scholarly Journals--Published
  • Oberg KC, Feenstra JM, Manske PR, Tonkin MA. 2010. Developmental Biology and Classification of Congenital Anomalies of the Hand and Upper Extremity. J Hand Surg 35A:2066–2076. ( 12/2010 - 1/2011 )
  • Oberg KC, Harris TE, Wongworawat MD, Wood VE. 2009.  Combined congenital radial and ulnar longitudinal deficiencies: A case report. J Hand Surgery 34A:1298–1302. ( 10/2009 )
  • Manske PR, Oberg KC. 2009. Classification and Developmental Biology of Congenital Anomalies of the Hand and Upper Extremity.  J Bone  Joint Surg 91(s4):3-18. ( 7/2009 )
  • Wang BW, Keith AL, Pira CU, Feenstra JM, Oberg KC. 2009.  Prostatic Hox genes: Expression during development and in TRAMP tumor cells.  FASEB J. 23: 470.6 ( 4/2009 )
  • Feenstra FM, Kanaya K, Pira CU, Oberg KC. 2009. . Lmx1b modulates extracellular matrix expression during limb dorsalization.  FASEB J. 23: 470.4 ( 4/2009 )
  • Komorowska-Timek E, Oberg KC, Timek TA, Gridley DS, Miles DA. 2009. The effect of AlloDerm envelopes on periprosthetic capsule formation with and without radiation.  Plast Reconstr Surg. 2009 Mar;123(3):807-16. ( 3/2009 )
  • Pira CU, Caltharp SA, Kanaya K, Manu SK, Greer LF, Oberg KC.  2009. Identification of Developmental Enhancers using Targeted Regional Electroporation (TREP) of Evolutionarily Conserved Regions.  In Proceedings of the 15th International Symposium on Bioluminescence and Chemiluminescence 2009, Kricka LJ, Stanley PE (eds). Chichester: Wiley, pp 319-323 ( 1/2009 )
  • Magaki S, Caltharp S, Westervelt D, Pira C, Greer LF, Oberg KC. 2009.  Characterization of a Nogo-associated enhancer.  J Invest Med 57:s107 ( 1/2009 )
  • Kanaya K. Feenstra JM, Pira CU, Oberg KC. 2008. Emx2 in limb dorsalization..  Dev Biol 319 (2): 509. #138 ( 7/2008 )
  • Magaki S, Raghavan R, Mueller C. Oberg KC, Vinters HV, Kirsch WM. "Iron, copper and iron regulatory protein 2 in Alzheimer?s disease and related dementias." Neurosci Lett 418.1 (2007): 72-76. ( 1/2007 ) Link...
    Accumulating evidence implicates a role for altered iron and copper metabolism in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). However, imbalances in the levels of the various forms of iron at different stages of AD have not been examined. In this pilot study we extracted and measured the levels of loosely bound, non-heme and total iron and copper in the frontal cortex and hippocampus of patients with mild-moderate AD (n=3), severe AD (n=8) and dementia with Lewy bodies (DLB, n=6), using graphite furnace atomic absorption spectrometry (GFAAS). Additionally, the expression of iron regulatory protein 2 (IRP2) was examined in relation to the pathological hallmarks of AD and DLB, amyloid plaques, neurofibrillary tangles (NFT), and Lewy bodies, by immunohistochemistry. We found significantly decreased loosely bound iron in the hippocampal white matter of mild-moderate and severe AD patients and a trend towards increased non-heme iron in the hippocampal gray matter of severe AD patients. Furthermore, decreased levels of total copper were seen in severe AD and DLB frontal cortex compared to controls, suggesting an imbalance in brain metal levels in both AD and DLB. The decrease in loosely bound iron in mild-moderate AD patients may be associated with myelin breakdown seen in the beginning stages of AD and implicates that iron dysregulation is an early event in AD pathogenesis.
  • Caltharp SA, Pira CU, Mishima N, Youngdale EN, McNeil DS, Liwnics BH, Oberg KC. "NOGO-A induction and localization during chick brain development indicates a role disparate from neurite outgrowth inhibition." BMC Development 7.32 (2007): 1-15. ( 1/2007 ) Link...
    BACKGROUND: Nogo-A, a myelin-associated protein, inhibits neurite outgrowth and abates regeneration in the adult vertebrate central nervous system (CNS) and may play a role in maintaining neural pathways once established. However, the presence of Nogo-A during early CNS development is counterintuitive and hints at an additional role for Nogo-A beyond neurite inhibition. RESULTS: We isolated chicken NOGO-A and determined its sequence. A multiple alignment of the amino acid sequence across divergent species, identified five previously undescribed, Nogo-A specific conserved regions that may be relevant for development. NOGO gene transcripts (NOGO-A, NOGO-B and NOGO-C) were differentially expressed in the CNS during development and a second NOGO-A splice variant was identified. We further localized NOGO-A expression during key phases of CNS development by in situ hybridization. CNS-associated NOGO-A was induced coincident with neural plate formation and up-regulated by FGF in the transformation of non-neural ectoderm into neural precursors. NOGO-A expression was diffuse in the neuroectoderm during the early proliferative phase of development, and migration, but localized to large projection neurons of the optic tectum and tectal-associated nuclei during architectural differentiation, lamination and network establishment. CONCLUSION: These data suggest Nogo-A plays a functional role in the determination of neural identity and/or differentiation and also appears to play a later role in the networking of large projection neurons during neurite formation and synaptogenesis. These data indicate that Nogo-A is a multifunctional protein with additional roles during CNS development that are disparate from its later role of neurite outgrowth inhibition in the adult CNS.
  • Gheorghe CP, Mohan S, Oberg KC, Longo LD. "Gene Expression Patterns in the Hypoxic Murine Placenta: A Role in Epigenesis?." Reproductive Sciences 14. (2007): 223-233. ( 1/2007 ) Link...
    Hypoxia has been identified as a major stress or in placental and fetal development. To test the hypothesis that hypoxic stress responses are associated with gene expression changes, the authors measured gene expression in the mouse placenta in response to 48 hours of hypoxia. Embryonic day 15.5 pregnant mice were exposed to 48 hours of hypoxia (10.5% O(2)), after which the Affymetrix Mouse 430A_2.0 array was used to measure gene expression changes in the placenta. The authors observed 171 probe sets, corresponding to 163 genes, that were regulated by hypoxia (P < .01). Ninety genes were upregulated, and 73 were downregulated. The authors functionally annotated the regulated genes and examined overrepresented functional categories. Among the upregulated and downregulated genes, several overrepresented functional categories were observed. Upregulated genes included those involved in metabolism, oxygen transport, proteolysis, cell death, metabolism of reactive oxygen species, and DNA methylation. Genes involved in transcription, cell cycle regulation, and cell structure were downregulated. Microarray analysis has allowed the description of the genetic responses to hypoxia in the mouse placenta. The observation that hypoxia upregulates reactive oxygen species metabolism, in conjunction with DNA methylation enzymes, suggests that hypoxia may contribute to long-term epigenetic changes in stressed fetal tissues and organs.
  • Naruse T, Takahara M, Takagi M, Oberg KC, Ogino T. "Busulfan-Induced Central Polydactyly, Syndactyly and Cleft Hand/Foot: A Common Mechanism of Disruption Leads to Divergent Phenotypes." Dev Growth Differ 49.6 (2007): 533-541. ( 1/2007 ) Link...
    The prevalence of clinical phenotypes that exhibit combinations of central polydactyly, syndactyly, or cleft hand or foot is higher than would be expected for random independent mutations. We have previously demonstrated that maternal ingestion of a chemotherapeutic agent, busulfan, at embryonic day 11 (E11) induces these defects in various combinations in rat embryo limbs. In an effort to determine the mechanism by which busulfan disrupts digital development, we examined cell death by Nile Blue staining and TdT-mediated dUTP nick end labeling (TUNEL) assays; we also carried out whole mount in situ hybridization for fibroblast growth factor-8 (Fgf8), bone morphogenetic protein-4 (Bmp4), and sonic hedgehog (Shh) to examine developmental pathways linked to these defects. In busulfan-treated embryos, diffuse cell death was evident in both ectoderm and mesoderm, peaking at E13. The increased cell death leads to regression of Fgf8 in the apical ectodermal ridge (AER) and Bmp4 and Shh in the underlying mesoderm. The subsequent pattern of interdigital apoptosis and cartilage condensation was variably disrupted. These results suggest that busulfan manifests its teratogenic effects by inducing cell death of both ectoderm and mesoderm, with an associated reduction in tissue and a disruption in the generation of patterning molecules during critical periods of digit specification.
  • Sasaki GH, Oberg KC, Tucker B, Gaston M. "The effectiveness and safety of topical PhotoActif phosphatidylcholine-based anti-cellulite gel and LED (red and near-infrared) light on Grade II-III thigh cellulite: A randomized, double-blinded study." J Cosmet Laser Ther 9.2 (2007): 87-96. ( 1/2007 ) Link...
    BACKGROUND: Cellulite of the upper lateral and posterior thighs and lower buttocks represents a common, physiological and unwanted condition whose etiologies and effective management are subjects of continued debate. OBJECTIVE: The purpose of this controlled, double-blinded study is to evaluate the efficacy and safety of a novel phosphatidylcholine-based, cosmeceutical anti-cellulite gel combined with a light-emitting diode (LED) array at the wavelengths of red (660 nm) and near-infrared (950 nm), designed to counter the possible mechanisms that purportedly accentuate the presence of thigh cellulite. METHODS: Nine healthy female volunteers with Grade II-III thigh cellulite were randomly treated twice daily with an active gel on one thigh and a placebo gel on the control thigh for 3 months. Twice weekly, each thigh was exposed for a 15-minute treatment with LED light for a total of 24 treatments. At 0, 6, and 12 weeks of the study the following clinical determinants were obtained: standardized digital photography, height and weight measurements, standardized thigh circumference tape measurements, pinch testing, body mass index (kg/m2), body fat analysis (Futrex-5500/XL near-infrared analyzer), and digital high-resolution ultrasound imaging of the dermal-adiposal border. In selected patients, full-thickness biopsies of the placebo and active-treated sites were obtained. At 18 months, repeat standardized digital photography, height and weight measurements, and body mass index measurements were obtained. RESULTS: At the end of 3 months, eight of nine thighs treated with the phosphatidylcholine-based, anti-cellulite gel and LED treatments were downgraded to a lower cellulite grade by clinical examination, digital photography, and pinch test assessment. Digital ultrasound at the dermal-adiposal interface demonstrated not only a statistically significant reduction of immediate hypodermal depth, but also less echo-like intrusions into the dermal layer. Three of six biopsies from thighs treated for 3 months with the active gel and LED treatments demonstrated less intrusion of subcutaneous fat into the papillary and reticular dermis. In nine placebo and LED-treated thighs and one of the actively treated thighs, minimal clinical changes were observed or measured by the clinical determinants throughout the 3-month study. At the month-18 evaluation period for the eight responsive thighs, five thighs reverted back to their original cellulite grading, while three thighs continued to maintain their improved status. Patients experienced minimal and transient side effects that included puritus, erythema and swelling. CONCLUSIONS: The results of this small but well-documented, randomized, double-blinded study affirms that eight of nine thighs with Grade II-III cellulite responded positively to a novel, combined 3-month treatment program of a phosphatidylcholine-based, anti-cellulite gel and LED exposure, as determined by the clinical determinants obtained. Patients experienced minimal and transient side effects. At the month-18 evaluation period (15 months after treatment), five responsive thighs reverted back to their original cellulite grading, indicating a need for maintenance treatment. Future studies are needed to verify these tentative positive observations.
  • Townsend Dominique, Brier-Jones Justin, Pira Charmaine, & Oberg Kerby. (2014). Role of EST2/ETV5 as transcription factors in the regulation of SHH by FGF. FASEB Journal, 28(1), . ( 4/2014 - Present )
  • Oberg Kerby. (2014). Review of the Molecular Development of the Thumb: Digit Primera. Clinical Orthopaedics & Related Research, 472(4), 1101-1105. ( 0/2014 - Present ) Link...
    Background: The thumb, or digit 1, is not a typical digit. In addition to its unusual mobility and function, its formation is also unusual. It is the last digit to form and the most commonly targeted when limb development is disrupted. The thumb domain is defined by the overlapping expression of HOXA13, TBX5, GLI3R, and HOXD13 and, importantly, by an absence of other distal HOXD transcription factors. This brief review, combining developmental biology and clinical genetics, discusses the current understanding of how the thumb domain is established. [ABSTRACT FROM AUTHOR] Copyright of Clinical Orthopaedics & Related Research is the property of Springer Science & Business Media B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
  • Haro Endika, Delgado Irene, Junco Marisa, Yamada Yoshihiko, Mansouri Ahmed, Oberg Kerby C, & Ros Marian A. (2014). Sp6 and Sp8 Transcription Factors Control AER Formation and Dorsal-Ventral Patterning in Limb Development. PLoS Genetics, 10(8), 1-16. ( 0/2014 - Present ) Link...
    The formation and maintenance of the apical ectodermal ridge (AER) is critical for the outgrowth and patterning of the vertebrate limb. The induction of the AER is a complex process that relies on integrated interactions among the Fgf, Wnt, and Bmp signaling pathways that operate within the ectoderm and between the ectoderm and the mesoderm of the early limb bud. The transcription factors Sp6 and Sp8 are expressed in the limb ectoderm and AER during limb development. Sp6 mutant mice display a mild syndactyly phenotype while Sp8 mutants exhibit severe limb truncations. Both mutants show defects in AER maturation and in dorsal-ventral patterning. To gain further insights into the role Sp6 and Sp8 play in limb development, we have produced mice lacking both Sp6 and Sp8 activity in the limb ectoderm. Remarkably, the elimination or significant reduction in Sp6;Sp8 gene dosage leads to tetra-amelia; initial budding occurs, but neither Fgf8 nor En1 are activated. Mutants bearing a single functional allele of Sp8 (Sp6‚??/‚??;Sp8+/‚??) exhibit a split-hand/foot malformation phenotype with double dorsal digit tips probably due to an irregular and immature AER that is not maintained in the center of the bud and on the abnormal expansion of Wnt7a expression to the ventral ectoderm. Our data are compatible with Sp6 and Sp8 working together and in a dose-dependent manner as indispensable mediators of Wnt/ő≤catenin and Bmp signaling in the limb ectoderm. We suggest that the function of these factors links proximal-distal and dorsal-ventral patterning. [ABSTRACT FROM AUTHOR] Copyright of PLoS Genetics is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
  • Feenstra J M, Kanaya K, Pira C U, Hoffman S E, Eppey R J, & Oberg K C. (2012). Detection of genes regulated by Lmx1b during limb dorsalization. Development Growth & Differentiation, 54(4), 451-462. ( 5/2012 - Present ) Link...
    Lmx1b is a homeodomain transcription factor that regulates dorsal identity during limb development. Lmx1b knockout (KO) mice develop distal ventralventral limbs. Although induction of Lmx1b is linked to Wnt7a expression in the dorsal limb ectoderm, the downstream targets of Lmx1b that accomplish limb dorsalization are unknown. To identify genes targeted by Lmx1b, we compared gene arrays from Lmx1b KO and wild type mouse limbs during limb dorsalization, i.e., 11.5, 12.5, and 13.5 days post coitum. We identified 54 target genes that were differentially expressed in all three stages. Several skeletal targets, including Emx2, Matrilin1 and Matrilin4, demonstrated a loss of scapular expression in the Lmx1b KO mice, supporting a role for Lmx1b in scapula development. Furthermore, the relative abundance of extracellular matrix-related soft tissue targets regulated by Lmx1b, such as collagens and proteoglycans, suggests a mechanism that includes changes in the extracellular matrix composition to accomplish limb dorsalization. Our study provides the most comprehensive characterization of genes regulated by Lmx1b during limb development to-date and provides targets for further investigation.
  • Oberg K C. (2011). Re: MM Al-Qattan Wnt pathways and upper limb anomalies J Hand Surg Eur 2011, 36: 9-22. Journal of Hand Surgery-European Volume, 36E(5), 434-434. ( 6/2011 - Present ) Link...
  • Oberg K C, Feenstra J M, Manske P R, & Tonkin M A. (2010). Developmental Biology and Classification of Congenital Anomalies of the Hand and Upper Extremity. Journal of Hand Surgery-American Volume, 35A(12), 2066-2076. ( 12/2010 - Present ) Link...
    Recent investigations into the mechanism of limb development have clarified the roles of several molecules, their pathways, and interactions Characterization of the molecular pathways that orchestrate limb development has provided insight into the etiology of many limb malformations In this review, we describe how the insights from developmental biology are related to clinically relevant anomalies and the current classification schemes used to define, categorize, and communicate patterns of upper limb malformations We advocate an updated classification scheme for upper limb anomalies that incorporates our current molecular perspective of limb development and the pathogenetic basis for malformations using dysmorphology terminology We anticipate that this scheme will improve the utility of a classification as a basis for diagnosis, treatment, and research (J Hand Surg 2010,35A 2066-2076 (C) 2010 Published by Elsevier Inc on behalf of the American Society for Surgery of the Hand)
  • Oberg K C, Harris T E, Wongworawat M D, & Wood V E. (2009). Combined Congenital Radial and Ulnar Longitudinal Deficiencies: Report of 2 Cases. Journal of Hand Surgery-American Volume, 34A(7), 1298-1302. ( 9/2009 - Present ) Link...
    Variation in longitudinal deficiencies is likely related to the timing and duration of an insult during early limb development. In experimental models, teratogenic insults induce ulnar deficiencies earlier in gestation than radial deficiencies. In this report, we describe the rare combination of right radial and left ulnar deficiencies in 2 cases. Interestingly, 1 case had a history of 2 separate and apparently distinct episodes of bleeding during early gestation, whereas the other demonstrated associated hematoma formation early in development. These cases also demonstrate the susceptibility for ulnar defects on the left and radial defects on the right. The authors discuss the relationship of prenatal insults on limb development and the mechanisms underlying longitudinal deficiencies. (J Hand Surg 2009;34A:1298-1302. (C) 2009 Published by Elsevier Inc. on behalf of the American Society for Surgery of the Hand.)
  • Komorowska-Timek E, Oberg K C, Timek T A, Gridley D S, & Miles D A. (2009). The effect of AlloDerm envelopes on periprosthetic capsule formation with and without radiation. , 123(3), 807-16. ( 3/2009 - Present ) Link...
    BACKGROUND: The pathobiology of radiation-induced periprosthetic capsular formation and factors that may ameliorate its development have not been fully elucidated. The authors hypothesized that AlloDerm would diminish radiation-induced capsular formation. METHODS: Two 5-ml implants were placed submuscularly in the backs of 41 rats. The right implant was wrapped with AlloDerm and the left remained bare. After 48 hours, 20 animals underwent irradiation to each implant, and 21 animals underwent no further treatment and served as controls. After 3 and 12 weeks, the capsules were harvested and submitted for tensile strength and histologic examination. Intraprosthetic pressures were measured in each implant at the time of surgery and when the animals were killed. RESULTS: The intraprosthetic pressure decrease was uniform among all groups at 3 and 12 weeks. Between 3 and 12 weeks, capsular tensile strength increased in nonirradiated bare implants. There was considerable invasion of nonirradiated AlloDerm by inflammatory infiltrates at 3 weeks, and AlloDerm thickness decreased over time. Cellular invasion of AlloDerm was decreased with irradiation at both time points. Capsular tensile strength and thickness of the irradiated bare and AlloDerm capsules did not change between 3 and 12 weeks. Radiation increased inflammation of bare capsules at 12 weeks, but it was significantly reduced in irradiated AlloDerm capsules. The majority of irradiated bare capsules developed pseudoepithelium, whereas AlloDerm protected capsules from this transformation. CONCLUSION: AlloDerm decreases radiation-related inflammation and delays or diminishes pseudoepithelium formation and thus may slow progression of capsular formation, fibrosis, and contraction.
  Non-Scholarly Journals
  • Oberg KC.  2008.  A word fitly spoken. December 17.  In: Morning Rounds: Daily Devotional Stories.. Hadley D (ed.). Loma Linda University Press, Loma Linda, CA. pp 351 ( 12/2008 )
  • Espinoza A J, Feenstra J, Pira C, & Oberg K. (2013). LMX1B-Regulated Nephrogenesis: A Role for Proteoglycans. FASEB Journal, 27, 1. ( 4/2013 - Present )
  • Coy S, Pira C U, & Oberg K C. (2013). Evaluation of the Regulatory Activity of the LSRB3 region of Limb Specific SHH Regulatory Region (LSSRR) in the Chicken Model. FASEB Journal, 27, 1. ( 4/2013 - Present )
  • Coggins A, Pira C U, Feenstra J M, & Oberg K C. (2013). Upregulation of sonic hedgehog by fibroblast growth factor: Is TFAP2C a downstream intermediate?. FASEB Journal, 27, 1. ( 4/2013 - Present )
  • Coggins A S, Pira C U, Feenstra J M, & Oberg K C. (2013). UP-REGULATION OF SONIC HEDGEHOG BY FIBROBLAST GROWTH FACTOR: THE ROLE OF TFAP2C, A DOWNSTREAM INTERMEDIATE. Journal of Investigative Medicine, 61(1), 190-190. ( 1/2013 - Present )
  • Espinoza A J, Feenstra J M, Pira C U, & Oberg K C. (2013). EXPRESSION OF LMX1B, KERATOCAN, LUMICAN AND DECORIN DURING NEPHROGENESIS. Journal of Investigative Medicine, 61(1), 121-122. ( 1/2013 - Present )
  • Schober J P, Pira C U, & Oberg K C. (2012). Identification of a regulatory region within the EMX2 locus that is active in the neural tube. Faseb Journal, 26, . ( 4/2012 - Present )
  • Van Hong A, Feenstra J M, Pira C U, & Oberg K C. (2012). Identification of a proteoglycan-associated regulatory region active during central nervous system development. Faseb Journal, 26, . ( 4/2012 - Present )
  • Stump R P, Feenstra J M, Castillo M A, Soriano S, & Oberg K C. (2012). The use of human embryonic kidney (HEK 293) cells to enhance characterization of the LMX1B pathway. Faseb Journal, 26, . ( 4/2012 - Present )
  • Kim D J H, Feenstra J M, Pira C U, & Oberg K C. (2012). UP-REGULATION OF TFAP2C BY FGF DURING SHH INDUCTION IN LIMB BUDS. Faseb Journal, 26, . ( 4/2012 - Present )
  • Bailey T W, Pira C U, & Oberg K C. (2012). FGF-INDUCED ACTIVATION OF THE LIMB SPECIFIC SHH REGULATORY REGION (LSSRR). Faseb Journal, 26, . ( 4/2012 - Present )
  • Bailey T W, Pira C, & Oberg K. (2012). FGF-INDUCED ACTIVATION OF THE LIMB SPECIFIC SHH REGULATORY REGION (LSSRR). Journal of Investigative Medicine, 60(1), 206-206. ( 1/2012 - Present )
  • Schober J P, Pira C U, & Oberg K C. (2012). IDENTIFICATION OF A REGULATORY REGION WITHIN THE EMX2 LOCUS THAT IS ACTIVE IN THE NEURAL TUBE AND DEVELOPING LIMB. Journal of Investigative Medicine, 60(1), 203-203. ( 1/2012 - Present )
  • Hundley E P, Pira C U, & Oberg K C. (2012). MOLECULAR INTERMEDIATES IN THE INDUCTION OF SHH BY FGF DURING LIMB DEVELOPMENT. Journal of Investigative Medicine, 60(1), 202-203. ( 1/2012 - Present )
  • Hong A V, Feenstra J M, Pira C U, & Oberg K C. (2012). IDENTIFICATION OF A PROTEOGLYCAN-ASSOCIATED REGULATORY REGION ACTIVE DURING CENTRAL NERVOUS SYSTEM DEVELOPMENT. Journal of Investigative Medicine, 60(1), 206-206. ( 1/2012 - Present )
  • Feenstra J, Estes M, & Oberg K. (2011). Proteoglycan gene expression during Lmx1b-directed limb dorsalization reveals disparate conservation. Developmental Biology, 356(1), 253-253. ( 8/2011 - Present ) Link...
  • Mattison G L, Steinman E D, Pira C U, & Oberg K C. (2011). UpRegulation of Lef1 during Fgf2 Mediated Induction of Shh Expression. Faseb Journal, 25, . ( 4/2011 - Present )
  • Rudisaile D G, Woods R O, Pira C U, Fallon J F, & Oberg K C. (2011). Sonic Hedgehog Promotes Patterned Regeneration in OZD Mutants. Faseb Journal, 25, . ( 4/2011 - Present )
  • Steinman E D, Mattison G L, Pira C U, & Oberg K C. (2011). DEFINING THE MECHANISM OF LIMB REGENERATION: A POTENTIAL NOVEL ROLE FOR BAMBI IN MEDIATING FGF-INDUCED SHH UP-REGULATION. Journal of Investigative Medicine, 59(1), 175-175. ( 1/2011 - Present )
  • Mattison G L, Steinman E D, Pira C U, & Oberg K C. (2011). INCREASED LEF1 EXPRESSION IMPLICATES THE WNT/beta-CATENIN PATHWAY IN THE MEDIATION OF FGF-INDUCED UP-REGULATION OF SHH. Journal of Investigative Medicine, 59(1), 175-175. ( 1/2011 - Present )
  • Estes M K, Feenstra J M, Pira C U, & Oberg K C. (2011). DISPARATE CONSERVATION OF GENE EXPRESSION IN LMX1B-DIRECTED LIMB DORSALIZATION. Journal of Investigative Medicine, 59(1), 174-175. ( 1/2011 - Present )
  • Willis B C, Pira C U, Caltharp S A, Kanaya K, Feenstra J M, & Oberg K C. (2010). Identification of a brain and neural tube specific enhancer associated with the expression of Emx2 during development. Developmental Biology, 344(1), 495-495. ( 8/2010 - Present ) Link...
  • Woods R O, Pira C U, Fallon J F, & Oberg K C. (2010). LIMB REGENERATION IN NORMAL AND OLIGOZEUGODACTYLY CHICKS. Journal of Investigative Medicine, 58(1), 160-161. ( 1/2010 - Present )
  • Woods R O, Pira C U, Fallon J F, & Oberg K C. (2010). LIMB REGENERATION IN NORMAL AND OLIGOZEUGODACTYLY CHICKS. Journal of Investigative Medicine, 58(1), 102-102. ( 1/2010 - Present )
  • Kanady J A, Austin A, Hopper A, Oberg K, Castelino-Prabhu S, Power G, & Blood A. (2010). NITRITE SUPPLEMENTATION FOR THE PREVENTION OF NECROTIZING ENTEROCOLITIS IN NEWBORN RAT PUPS. Journal of Investigative Medicine, 58(1), 186-186. ( 1/2010 - Present )
  • Huynh A N, Martin C M, Pira C U, & Oberg K C. (2010). A HOX REGULATORY MODULE WITHIN THE LIMB SPECIFIC SHH REGULATORY REGION EXHIBITS DUAL ENHANCER AND INHIBITOR ACTIVITY. Journal of Investigative Medicine, 58(1), 160-160. ( 1/2010 - Present )
  • Magaki S, Caltharp S, Westervelt D, Pira C, Greer L F, & Oberg K C. (2009). CHARACTERIZATION OF A NOGO-ASSOCIATED ENHANCER. Journal of Investigative Medicine, 57(1), 152-153. ( 1/2009 - Present )