Jon Cogan

ORCID: 0000-0001-9327-8711
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Skin and Cellular Biology Research
  • Autoimmune Bullous Skin Diseases
  • Cell Adhesion Molecules Research
  • Prostate Cancer Treatment and Research
  • Bone Metabolism and Diseases
  • Dermatological and Skeletal Disorders
  • Contact Dermatitis and Allergies
  • Bone health and treatments
  • Estrogen and related hormone effects
  • Cancer-related gene regulation
  • Nail Diseases and Treatments
  • Plant Reproductive Biology
  • Peptidase Inhibition and Analysis
  • Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
  • Cellular Mechanics and Interactions
  • Hair Growth and Disorders
  • Ubiquitin and proteasome pathways
  • Wnt/β-catenin signaling in development and cancer
  • Hormonal and reproductive studies
  • Cancer, Lipids, and Metabolism
  • Silk-based biomaterials and applications
  • Bone and Dental Protein Studies
  • 14-3-3 protein interactions
  • Genomics and Chromatin Dynamics
  • Genetic Syndromes and Imprinting

University of Southern California
2014-2024

VasGene Therapeutics (United States)
2023-2024

Southern California University for Professional Studies
2013

Keck Hospital of USC
2008

United States Department of Veterans Affairs
1979

National Institute of Arthritis and Musculoskeletal and Skin Diseases
1979

National Institutes of Health
1979

National Cancer Institute
1979

The androgen receptor (AR) is a steroid-activated transcription factor that binds at specific DNA locations and plays key role in the etiology of prostate cancer. While numerous studies have identified clear connection between AR binding expression target genes for limited number loci, high-throughput elucidation these sites allows deeper understanding complexities this process.We mapped 189 occupied regions (ARORs) 1,388 histone H3 acetylation (AcH3) loci to 3% continuous stretch human...

10.1371/journal.pone.0003645 article EN cc-by PLoS ONE 2008-11-08

Recessive dystrophic epidermolysis bullosa (RDEB) is an incurable disease caused by mutations in the gene encoding type VII collagen, major component of anchoring fibrils (AF). We previously demonstrated that gentamicin produced functional collagen RDEB cells harboring nonsense mutations. Herein, we determined whether topical or intradermal administration induces and AFs patients.A double-blind, placebo-controlled pilot trial assessed safety efficacy 5 patients with The arm tested 0.1%...

10.1172/jci92707 article EN Journal of Clinical Investigation 2017-07-09

The androgen receptor (AR) plays critical roles in both androgen-dependent and castrate-resistant prostate cancer (PCa). However, little is known about AR target genes that mediate the receptor's disease progression.Using Chromatin Immunoprecipitation (ChIP) Display, we discovered 19 novel loci occupied by castrate resistant C4-2B PCa cells. Only four of AR-occupied regions were within 10-kb 5'-flanking regulatory sequences. Three located up to 4-kb 3' nearest gene, eight intragenic gene...

10.1186/1476-4598-6-39 article EN cc-by Molecular Cancer 2007-06-06

Herlitz junctional epidermolysis bullosa (H-JEB) is an incurable, devastating, and mostly fatal inherited skin disease for which there only supportive care. H-JEB caused by loss-of-function mutations in LAMA3, LAMB3, or LAMC2, leading to complete loss of laminin 332, the major component anchoring filaments, mediate epidermal-dermal adherence. LAMB3 (laminin β3) account 80% patients with H-JEB, ∼95% H-JEB-associated are nonsense premature termination codons (PTCs). In this study, we evaluated...

10.1073/pnas.1803154115 article EN Proceedings of the National Academy of Sciences 2018-06-26

Patients with recessive dystrophic epidermolysis bullosa (RDEB) have severe, incurable skin fragility, blistering, and multiple wounds due to mutations in the gene encoding type VII collagen (C7), major component of anchoring fibrils mediating epidermal-dermal adherence. Nearly 10–25% RDEB patients carry nonsense leading premature stop codons (PTCs) that result truncated C7. In this study, we evaluated feasibility using aminoglycosides suppress PTCs induce C7 expression two keratinocyte cell...

10.1038/mt.2014.140 article EN cc-by-nc-nd Molecular Therapy 2014-08-26

Generalized severe junctional epidermolysis bullosa (GS-JEB) is an incurable and fatal autosomal recessively inherited blistering skin disease caused by mutations in the LAMA3, LAMB3, or LAMC2 genes. Most of these are nonsense that create premature termination codons lead to impaired production functional laminin 332, a protein needed for epidermal-dermal adherence. Gentamicin induces readthrough restores full-length various genetic diseases. Using primary keratinocytes from three GS-JEB...

10.1016/j.ymthe.2020.03.006 article EN cc-by-nc-nd Molecular Therapy 2020-03-17

Recessive dystrophic epidermolysis bullosa (RDEB) is an incurable widespread blistering skin disorder caused by mutations in the gene encoding for type VII collagen (C7), major component of anchoring fibrils.

10.1093/bjd/ljae063 article EN British Journal of Dermatology 2024-02-16

We investigated the role of Lef1, one four transcription factors that transmit Wnt signaling to genome, in regulation bone mass. Microcomputed tomographic analysis 13- and 17-week-old mice revealed significantly reduced trabecular mass Lef1+/− females compared littermate wild-type females. This was attributable decreased osteoblast activity formation as indicated by histomorphometric remodeling. In contrast females, unaffected Lef1 haploinsufficiency males. Similarly, were substantially more...

10.1371/journal.pone.0005438 article EN cc-by PLoS ONE 2009-05-01

Junctional epidermolysis bullosa (JEB) is an incurable blistering skin disorder with high infant mortality often caused by nonsense variants in the genes that encode laminin 332.To evaluate safety and outcomes following intravenous gentamicin readthrough therapy subsequent 332 expression patients JEB.This open-label, pilot nonrandomized clinical trial assessed 1 course of low- or high-dose gentamicin, including follow-up at 30 90 days after treatment. Five pediatric JEB (2 intermediate 3...

10.1001/jamadermatol.2021.5992 article EN JAMA Dermatology 2022-03-02

Abstract BACKGROUND The androgen receptor (AR) plays a pivotal role in prostate cancer (PCa) initiation and progression. To date, studies have focused disproportionately on androgen‐stimulated genes such as prostate‐specific antigen (PSA), while repressed gained little attention, even though they too may be involved regulating cell growth, differentiation, apoptosis. METHODS ChIP Display was used to identify putative AR target the ablation‐resistant human PCa line, C4‐2B. Quantitative...

10.1002/pros.20623 article EN The Prostate 2007-07-11

Periostin, an extracellular matrix macromolecule implicated in tumorigenesis, serves as a prognostic marker for many cancer types. However, there are no data on periostin expression cutaneous squamous cell carcinoma (cSCC). This study examined patients with cSCC and explored its clincopathological relationship prognosis. Using immunohistochemistry ImageJ analysis, we compared 95 cSCCs across spectrum of aggressiveness: situ (SCCIS) (n = 25), low-risk (LR-cSCC) 26), high-risk (HR-cSCC) 38),...

10.1111/exd.14281 article EN Experimental Dermatology 2021-01-16

Abstract Krox20 is expressed in osteoblasts and chondrocytes, required for trabecular bone formation during embryogenesis. Here we show by RT‐qPCR Western blot analysis that up‐regulated late stages of osteoblast differentiation culture. Glucocorticoids (GCs) rapidly inhibit the expression as well its co‐activator, HCF‐1, resulting inhibition Osteocalcin Krox20‐binding Enhancer (OKE). GCs also EGR1, EGR3, EGR4. OKE activity, which dependent on presence Runx2, was independent osteocalcin...

10.1002/jcb.21587 article EN Journal of Cellular Biochemistry 2007-10-31

Metabolism of T4-binding globulin (TBG) was studied in rhesus monkeys after iv injection trace amounts 125I-labeled TBG. The animals were investigated during a control period, experimentally induced hyperthyroidism (T3 toxicosis), and hypothyroidism (6 weeks thyroidectomy). Kinetic parameters calculated from serum TBG levels (measured by RIA), [125I]PBI (shown to represent circulating radioactive TBG), daily urinary excretion radioiodide. A compartmental model used analyze the urine data...

10.1210/endo-104-1-175 article EN Endocrinology 1979-01-01

Abstract BACKGROUND The androgen receptor (AR) plays roles in prostate development and cancer (PCa). In response to androgens, the AR binds androgen‐response elements (AREs) modulate gene transcription. responses of such genes are dependent on cellular milieu sequences around AREs, which attract other transcription factors. Previously, bioinformatic analysis 62 AR‐occupied regions (ARORs) PCa cells revealed enrichment for both AREs a TTGGCAAATA‐like motif. We undertook present study...

10.1002/pros.20893 article EN The Prostate 2008-12-03

4577 Background: B2 is a ligand for EphB4 (B4) which enhances tumor invasion, proliferation, survival and promotes angiogenesis. TCGA data (N= 409) bladder cancer patients (pts) showed high expression (34%) had poor OS vs. low (66%) (Hazard Ratio- HR- 0.7 p=0.02). Our phase II trial of sEphB4-HSA, inhibitor, combined with pembrolizumab in pre-treated mUC (N=70) an objective response rate (ORR) 37%. Pts 52% ORR 24% complete (CR) (JCO PMID 35984996). This retrospective study examined the to...

10.1200/jco.2024.42.16_suppl.4577 article EN Journal of Clinical Oncology 2024-06-01

10.1016/j.jid.2016.02.423 article EN publisher-specific-oa Journal of Investigative Dermatology 2016-04-28

4575 Background: B2 is a ligand for EphB4 which enhances tumor invasion, proliferation, survival and promotes angiogenesis. A prior analysis of TCGA data from 409 muscle invasive bladder cancer (MIBC) patients (pts) demonstrated that high (34%) gene expression had poor vs. low (66%) (Hazard Ratio 0.7 p = 0.02). Our phase II trial sEphB4-HSA (JCO PMID 35984996) targets B2, in combination with pembrolizumab previously treated mUC (N=70) an objective response rate (ORR) 37%. Among pts ORR was...

10.1200/jco.2023.41.16_suppl.4575 article EN Journal of Clinical Oncology 2023-06-01
Coming Soon ...