Rob C Smart

TIN2 is an architectural protein that facilitates TRF2-mediated trans- and cis-interactions on telomeric DNA

NUCLEIC ACIDS RESEARCH, 49(22), 13000–13018.

Measurement of Novel, Drinking Water-Associated PFAS in Blood from Adults and Children in Wilmington, North Carolina

ENVIRONMENTAL HEALTH PERSPECTIVES, 128(7).

C/EBP beta suppresses keratinocyte autonomous type 1 IFN response and p53 to increase cell survival and susceptibility to UVB-induced skin cancer

CARCINOGENESIS, 40(9), 1099–1109.

C/EBPβ deletion in oncogenic Ras skin tumors is a synthetic lethal event

Cell Death & Disease, 9(11).

Carcinogenesis

In R. C. Smart & E. Hodgson (Eds.), Molecular and Biochemical Toxicology (5th ed.). Hoboken, NJ: J Wiley and Sons.

Molecular Techniques in the Study of Gene Function

In R. C. Smart & E. Hodgson (Eds.), Molecular and Biochemical Toxicology (5th ed.). Hoboken, NJ: J Wiley and Sons.

Molecular and Biochemical Toxicology

(5th ed.). Hoboken, NJ: J. Wiley and Sons.

Molecular and Biochemical Toxicology

(ed.). J. Wiley and Sons.

Molecular and Biochemical Toxicology: Definition and Scope

In R. C. Smart & E. Hodgson (Eds.), Molecular and Biochemical Toxicology (5th ed.). Hoboken, NJ: J Wiley and Sons.

Long noncoding RNA lincRNA-p21 is the major mediator of UVB-induced and p53-dependent apoptosis in keratinocytes

CELL DEATH & DISEASE, 6.

C/EBPα regulates CRL4Cdt2-mediated degradation of p21 in response to UVB-induced DNA damage to control the G1/S checkpoint

Cell Cycle, 13(22), 3602–3610.

C/EBP alpha Expression Is Downregulated in Human Nonmelanoma Skin Cancers and Inactivation of C/EBP alpha Confers Susceptibility to UVB-Induced Skin Squamous Cell Carcinomas

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 131(6), 1339–1346.

CD34 antigen: Determination of specific sites of phosphorylation in vitro and in vivo

INTERNATIONAL JOURNAL OF MASS SPECTROMETRY, 301(1-3), 12–21.

Control of skin cancer by the circadian rhythm

Proceedings of the National Academy of Sciences, 108(46), 18790–18795.

PTEN Positively Regulates UVB-Induced DNA Damage Repair

CANCER RESEARCH, 71(15), 5287–5295.

Ablation of TAK1 Upregulates Reactive Oxygen Species and Selectively Kills Tumor Cells

Cancer Research, 70(21), 8417–8425.

C/EBP alpha and C/EBP beta Are Required for Sebocyte Differentiation and Stratified Squamous Differentiation in Adult Mouse Skin

PLOS ONE, 5(3).

Chemical Carcinogenesis and Mutagenesis

In E. Hodgson (Ed.), Modern Toxicology (4th ed.). New York: J. Wiley and Sons.

Overexpression of Transcription Factor Sp2 Inhibits Epidermal Differentiation and Increases Susceptibility to Wound- and Carcinogen-Induced Tumorigenesis

CANCER RESEARCH, 70(21), 8507–8516.

RSK-Mediated Phosphorylation in the C/EBP beta Leucine Zipper Regulates DNA Binding, Dimerization, and Growth Arrest Activity

MOLECULAR AND CELLULAR BIOLOGY, 30(11), 2621–2635.

C/EBP alpha expression is partially regulated by C/EBP beta in response to DNA damage and C/EBP alpha-deficient fibroblasts display an impaired G(1) checkpoint

ONCOGENE, 28(36), 3235–3245.

C/EBP beta represses p53 to promote cell survival downstream of DNA damage independent of oncogenic Ras and p19(Arf)

CELL DEATH AND DIFFERENTIATION, 15(11), 1734–1744.

Carcinogenesis

In Molecular and Biochemical Toxicology (4th ed., pp. 537–586).

Molecular and Biochemical Toxicology

Molecular and Biochemical Toxicology: Definition and Scope

In R. C. Smart & E. Hodgson (Eds.), Molecular and Biochemical Toxicology (4th ed., pp. 1–4).

Overview of Molecular Techniques in Toxicology: Genes and Transgenes

In R. C. Smart & E. Hodgson (Eds.), Molecular and Biochemical Toxicology (4th ed., pp. 5–24).

Decreased survival of C/EBP beta-deficient keratinocytes is due to aberrant regulation of p53 levels and function

ONCOGENE, 26(3), 360–367.

Genetic ablation of CCAAT/Enhancer binding protein alpha in epidermis reveals its role in suppression of epithelial tumorigenesis

CANCER RESEARCH, 67(14), 6768–6776.

Conditional ablation of C/EBP beta demonstrates its keratinocyte-specific requirement for cell survival and mouse skin tumorigenesis

ONCOGENE, 25(8), 1272–1276.

TAK1 is a master regulator of epidermal homeostasis involving skin inflammation and apoptosis

JOURNAL OF BIOLOGICAL CHEMISTRY, 281(28), 19610–19617.

Diminished expression of C/EBP alpha in skin carcinomas is linked to oncogenic Ras and reexpression of C/EBP alpha in carcinoma cells inhibits proliferation

Cancer Research, 65(3), 861–867.

C/EBP alpha is a DNA damage-inducible p53-regulated mediator of the G(1) checkpoint in keratinocytes

MOLECULAR AND CELLULAR BIOLOGY, 24(24), 10650–10660.

Cell cycle-dependent phosphorylation of C/EBP beta mediates oncogenic cooperativity between C/EBP beta and H-Ras(V12)

MOLECULAR AND CELLULAR BIOLOGY, 24(17), 7380–7391.

Chemical Carcinogenesis

In E. Hodgson (Ed.), A Textbook of Modern Toxicology (pp. 225–250).

Introduction to Biochemical and Molecular Methods in Toxicology

In E. Hodgson (Ed.), A Textbook of Modern Toxicology (pp. 13–22).

Lithium stabilizes the CCAAT/enhancer-binding protein alpha (C/EBP alpha) through a glycogen synthase kinase 3 (GSK3)-independent pathway involving direct inhibition of proteasomal activity

JOURNAL OF BIOLOGICAL CHEMISTRY, 278(22), 19674–19681.

Method of treating alopecia

Washington, DC: U.S. Patent and Trademark Office.

Method of treating alopecia

(Vol. 6, 555, 532). Vol. 6, 555, 532. Washington, DC: U.S. Patent and Trademark Office.

17 beta-estradiol is a hormonal regulator of mirex tumor promotion sensitivity in mice

TOXICOLOGICAL SCIENCES, 69(1), 42–48.

CCAAT/enhancer binding protein-beta is a mediator of keratinocyte survival and skin tumorigenesis involving oncogenic Ras signaling

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 99(1), 207–212.

Deficiency of either cyclooxygenase (COX)-1 or COX-2 alters epidermal differentiation and reduces mouse skin tumorigenesis

Cancer Research, 62(12), 3395–3401.

Biochemical Toxicology: Definition and Scope

In E. Hodgson & R. C. Smart (Eds.), Introduction to Biochemical Toxicology (pp. 1–10). New York: J. Wiley and Sons.

Carcinogenesis

In E. Hodgson & R. C. Smart (Eds.), Introduction to Biochemical Toxicology (3rd ed., pp. 343–398). New York: J. Wiley and Sons.

Introduction to Biochemical Toxicology

(3rd ed.). New York: J. Wiley and Sons.

Introduction to Biochemical Toxicology

(ed.). J. Wiley and Sons.

Method of treating alopecia

Washington, DC: U.S. Patent and Trademark Office.

Method of treating alopecia

(Vol. 6, 204, 258). Vol. 6, 204, 258. Washington, DC: U.S. Patent and Trademark Office.

Molecular Techniques in Toxicology

In E. Hodgson & R. C. Smart (Eds.), Introduction to Biochemical Toxicology (3rd ed., pp. 11–32). New York: J. Wiley and Sons.

Protein kinase C-alpha coordinately regulates cytosolic phospholipase A(2) activity and the expression of cyclooxygenase-2 through different mechanisms in mouse keratinocytes

MOLECULAR PHARMACOLOGY, 59(4), 860–866.

17 beta-Estradiol and ICI-182780 regulate the hair follicle cycle in mice through an estrogen receptor-alpha pathway

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 278(2), E202–E210.

A multihit, multistage model of chemical carcinogenesis

CARCINOGENESIS, 20(9), 1837–1844.

C/EBP beta modulates the early events of keratinocyte differentiation involving growth arrest and keratin 1 and keratin 10 expression

Molecular and Cellular Biology, 19(10), 7181–7190.

Correlation between expression of peroxisome proliferator-activated receptor beta and squamous differentiation in epidermal and tracheobronchial epithelial cells

MOLECULAR AND CELLULAR ENDOCRINOLOGY, 147(1-2), 85–92.

Effects of 17-beta-estradiol and ICI 182 780 on hair growth in various strains of mice

Smart, R. C., Oh, H. S., Chanda, S., & Robinette, C. L. (1999, December). JOURNAL OF INVESTIGATIVE DERMATOLOGY SYMPOSIUM PROCEEDINGS, Vol. 4, pp. 285–289.

Methods of treating alopecia

Washington, DC: U.S. Patent and Trademark Office.

Methods of treating alopecia

(Vol. 5, 965, 551). Vol. 5, 965, 551. Washington, DC: U.S. Patent and Trademark Office.

Overexpression of protein kinase C-[alpha] in the epidermis of transgenic mice results in striking alterations in phorbol ester-induced inflammation and COX-2, MIP-2, and TNF-[alpha] but not tumor promotion

Journal of Cell Science, 112(20), 3497–3506.

Expression of CCAAT/enhancer binding proteins (C/EBP) is associated with squamous differentiation in epidermis and isolated primary keratinocytes and is altered in neoplasms

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 110(6), 939–945.

On the effect of estrogen receptor agonists and antagonists on the mouse hair follicle cycle

Smart, R. C., & Oh, H. S. (1998, July).

Evidence that mirex promotes a unique population of epidermal cells that cannot be distinguished by their mutant Ha ras genotype

Molecular Carcinogenesis, 20(1), 115–124.

An estrogen receptor pathway regulates the telogen-anagen hair follicle transition and influences epidermal cell proliferation.

Proceedings of the National Academy of Sciences, 93(22), 12525–12530.

Epidermal Protein Kinase C-β2 Is Highly Sensitive to Downregulation and Is Exclusively Expressed in Langerhans Cells: Downregulation Is Associated with Attenuated Contact Hypersensitivity

Journal of Investigative Dermatology, 107(3), 354–359.

Localization and Expression of Cornifin-α/SPRR1 in Mouse Epidermis, Anagen Follicles, and Skin Neoplasms

Journal of Investigative Dermatology, 106(4), 647–654.

Genetic alterations cooperate with v-Ha-ras to accelerate multistage carcinogenesis in TG.AC transgenic mouse skin

Cancer Research, 55(14), 3171–3178.

Lack of effect of retinoic acid and fluocinolone acetonide on mirex tumor promotion indicates a novel mirex mechanism

Carcinogenesis, 16(9), 2199–2204.

SYNERGISTIC INTERACTION BETWEEN THE NONPHORBOL ESTER-TYPE PROMOTER MIREX AND 12-O-TETRADECANOYLPHORBOL-13-ACETATE IN MOUSE SKIN TUMOR PROMOTION

CARCINOGENESIS, 15(1), 47–52.

Carcinogenesis

In E. Hodgson & P. E. Levi (Eds.), Biochemical Toxicology (2nd ed., pp. 381–414). Norwalk, CT: Appleton and Lange.

Characterization of benzo[a]pyrene-initiated mouse skin papillomas for Ha-ras mutations and protein kinase C levels

Carcinogenesis, 14(11), 2289–2295.

Characterization of skin tumor promotion by mirex: structure-activity relationships, sexual dimorphism and presence of Ha-ras mutation

Carcinogenesis, 14(6), 1155–1160.

Diacylglycerol is an effector of the clonal expansion of cells containing activated Ha-ras genes

Carcinogenesis, 14(12), 2645–2648.

MINIMAL ROLE OF ENHANCED CELL-PROLIFERATION IN SKIN TUMOR PROMOTION BY MIREX - A NONPHORBOL ESTER-TYPE PROMOTER

MEYER, S. A., MOSER, G. J., MONTEIRORIVIERE, N. A., & SMART, R. C. (1993, December). ENVIRONMENTAL HEALTH PERSPECTIVES, Vol. 101, pp. 265–269.

Alterations in protein kinase C isozymes α and β² in activated Ha-ras containing papillomas in the absence of an increase in diacyiglycerol

Carcinogenesis, 13(7), 1113–1120.

The chlorinated pesticide, mirex is a novel non-phorbol ester tumor promoter in mouse skin

Cancer Research, 52(3), 631–636.

EFFECT OF ASCORBIC-ACID AND ITS SYNTHETIC LIPOPHILIC DERIVATIVE ASCORBYL PALMITATE ON PHORBOL ESTER INDUCED SKIN-TUMOR PROMOTION IN MICE

AMERICAN JOURNAL OF CLINICAL NUTRITION, 54(6), S1266–S1273.

Pesticides, tumor promotion and risk assessment in Pesticides and the Future: Toxicological Studies of Risks and Benefits

In E. Hodgson, R. M. Roe, & N. Motoyama (Eds.), Reviews in Pesticides I (pp. 349–357).

Differential down-regulation of epidermal protein kinase C (PKC) by tetradecanoylphorbol-13-acetate and diacylglycerol: Association with epidermal hyperplasia and tumor promotion

Cancer Research, 50, 5740–5745.

Comparison of epidermal protein kinase C activity, ornithine decarboxylase induction and DNA synthesis stimulated by TPA or dioctanoylglycerol in mouse strains with differing susceptibility to TPA-induced tumor promotion

Carcinogenesis, 10(5), 833–838.

Hepatic tumor-promoting chlorinated hydrocarbons stimulate protein kinase C activity

Carcinogenesis, 10(5), 851–856.

Synthetic lipid second messenger, sn-1,2-didecanoylglycerol: A complete tumor promoter in mouse skin

Cancer Research, 49(16), 4455–4458.

COMPARISON OF THE EFFECT OF SN-1,2-DIDECANOYLGLYCEROL AND 12-O-TETRADECANOYLPHORBOL-13-ACETATE ON CUTANEOUS MORPHOLOGY, INFLAMMATION AND TUMOR PROMOTION IN CD-1 MICE

CARCINOGENESIS, 9(12), 2221–2226.

Inhibitory effect of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on tumor promotion in mouse skin by 12-o-tetradecanoylphorbol-13-acetate

Cancer Research, 48(21), 5941–5946.

Ascorbic Acid, Alcohol, and Environmental Chemicals

Annals of the New York Academy of Sciences, 498(1 Third Confere), 364–388.

Characterization of purified DT-diaphorase from liver cytosol of 3-methylcholanthrene-treated rats

Chemica Scripta, 27A:49-54.

Inhibition of 12-O-Tetradecanoylphorbol-13-acetate Induction of Ornithine Decarboxylase Activity, DNA Synthesis, and Tumor Promotion in Mouse Skin by Ascorbic Acid and Ascorbyl Palmitate

Cancer Research, 47(24, Part 1), 6633–6638.

Disposition of the naturally occurring antimutagenic plant phenol, ellagic acid, and its synthetic derivatives, 3-O-decylellagic acid and 3, 3'-di-O-methylellagic acid in mice

Carcinogenesis, 7(10), 1663–1667.

Effect of dietary ascorbate on covalent binding of benzene to bone marrow and hepatic tissue in vivo

Biochemical Pharmacology, 35(18), 3180–3182.

Effect of ellagic acid and 3-O-decylellagic acid on the formation of benzo[a]pyrene-derived DNA adducts in vivo and on the tumorigenicity of 3-methylcholanthrene in mice

Carcinogenesis, 7(10), 1669–1675.

sn-l, 2-Diacylglycerols mimic the effects of 12-0-tetradecanoylphorbol-13-acetate in vivo by inducing biochemical changes associated with tumor promotion in mouse epidermis

Carcinogenesis, 7(11), 1865–1870.

Effect of ascorbate on covalent binding of benzene and phenol metabolites to isolated tissue preparations

Toxicology and Applied Pharmacology, 77(2), 334–343.

Ascorbic acid as it relates to the metabolism of drugs and environmental chemicals

In M. Wimick (Ed.), Nutrition in the 20th Century (pp. 21–36). New York: John Wiley and Sons.

DT-Diaphorase and peroxidase influence the covalent binding of the metabolites of phenol, the major metabolite of benzene

Molecular Pharmacology, 26(1), 105–111.