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Article ; Online: Systematic parameter errors in inspiraling neutron star binaries.

Favata, Marc

2014 Volume 112, Issue 10, Page(s) 101101

Abstract: The coalescence of two neutron stars is an important gravitational wave source for LIGO and other detectors. Numerous studies have considered the precision with which binary parameters (masses, spins, Love numbers) can be measured. Here I consider the ... ...

Abstract	The coalescence of two neutron stars is an important gravitational wave source for LIGO and other detectors. Numerous studies have considered the precision with which binary parameters (masses, spins, Love numbers) can be measured. Here I consider the accuracy with which these parameters can be determined in the presence of systematic errors due to waveform approximations. These approximations include truncation of the post-Newtonian (PN) series and neglect of neutron star (NS) spin, tidal deformation, or orbital eccentricity. All of these effects can yield systematic errors that exceed statistical errors for plausible parameter values. In particular, neglecting spin, eccentricity, or high-order PN terms causes a significant bias in the NS Love number. Tidal effects will not be measurable with PN inspiral waveforms if these systematic errors are not controlled.
Language	English
Publishing date	2014-03-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	208853-8
ISSN	1079-7114 ; 0031-9007
ISSN (online)	1079-7114
ISSN	0031-9007
DOI	10.1103/PhysRevLett.112.101101
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Article: Identification of pAKT as a pharmacodynamic marker for MER kinase in human melanoma G361 cells.

Chen, Yaoyu / Favata, Margaret / Pusey, Michelle / Li, Jun / Lo, Yvonne / Ye, Min / Wynn, Richard / Wang, Xiaozhao / Yao, Wenqing / Chen, Yingnan

Biomarker research

2020 Volume 8, Page(s) 4

Abstract: Background: The MER signaling pathway represents an attractive therapeutic target for human cancers. Growth arrest-specific protein 6 (GAS6)-induced MER phosphorylation is often unstable and difficult to detect without pervanadate pretreatment in human ... ...

Abstract	Background: The MER signaling pathway represents an attractive therapeutic target for human cancers. Growth arrest-specific protein 6 (GAS6)-induced MER phosphorylation is often unstable and difficult to detect without pervanadate pretreatment in human cancer cells, posing a challenge for the development of selective MER kinase inhibitors. Here, we identified phosphorylated AKT (pAKT) as a specific pharmacodynamic marker for MER kinase inhibitors in human melanoma G361 cells. Methods: The expression of MER, TYRO3, and AXL were profiled among multiple human cancer cells. To determine whether they play a role in the activation of pAKT, MER and TYRO3 were selectively depleted by small, interfering RNA knockdown. In addition, using AKT phosphorylation as a readout, a high-throughput cell-based assay was established in G361 cells for evaluation of the potency of potential inhibitors of MER pathway activation. Results: We demonstrated that high levels of MER and TYRO3, but not AXL, were expressed in G361 cells. In these cells, pAKT was induced by GAS6 treatment, which could be reversed by AXL/MER inhibitors. We showed that GAS6-induced pAKT is only dependent on MER kinase, but not TYRO3, in G361 cells. Furthermore, we observed a correlation in potency between inhibition of pAKT in G361 cells and pMER in MER-overexpressing Ba/F3 cells by these inhibitors. Conclusions: In summary, we have demonstrated that GAS6-induced pAKT is a possible pharmacodynamic marker for the inhibition of MER kinase, and we have successfully developed a cell-based functional assay for screening small-molecule inhibitors of MER kinase for potential therapeutic utility in treating GAS6/MER-deregulated human cancers.
Language	English
Publishing date	2020-02-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2699926-2
ISSN	2050-7771
ISSN	2050-7771
DOI	10.1186/s40364-020-0184-9
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Article: A Potent and Selective Dual Inhibitor of AXL and MERTK Possesses Both Immunomodulatory and Tumor-Targeted Activity.

Frontiers in oncology

2020 Volume 10, Page(s) 598477

Abstract: TYRO3, AXL, and MERTK constitute the TAM family of receptor tyrosine kinases, which play important roles in tumor growth, survival, cell adhesion, as well as innate immunity, phagocytosis, and immune-suppressive activity. Therefore, targeting both AXL ... ...

Abstract	TYRO3, AXL, and MERTK constitute the TAM family of receptor tyrosine kinases, which play important roles in tumor growth, survival, cell adhesion, as well as innate immunity, phagocytosis, and immune-suppressive activity. Therefore, targeting both AXL and MERTK kinases may directly impact tumor growth and relieve immunosuppression. We describe here the discovery of INCB081776, a potent and selective dual inhibitor of AXL and MERTK that is currently in phase 1 clinical trials. In cellular assays, INCB081776 effectively blocked autophosphorylation of AXL or MERTK with low nanomolar half maximal inhibitory concentration values in tumor cells and Ba/F3 cells transfected with constitutively active AXL or MERTK. INCB081776 inhibited activation of MERTK in primary human macrophages and partially reversed M2 macrophage-mediated suppression of T-cell proliferation, which was associated with increased interferon-γ production.
Language	English
Publishing date	2020-12-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2020.598477
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Article ; Online: Preclinical characterization of itacitinib (INCB039110), a novel selective inhibitor of JAK1, for the treatment of inflammatory diseases.

European journal of pharmacology

2020 Volume 885, Page(s) 173505

Abstract: Pharmacological modulation of the Janus kinase (JAK) family has achieved clinically meaningful therapeutic outcomes for the treatment of inflammatory and hematopoietic diseases. Several JAK1 selective compounds are being investigated clinically to ... ...

Abstract	Pharmacological modulation of the Janus kinase (JAK) family has achieved clinically meaningful therapeutic outcomes for the treatment of inflammatory and hematopoietic diseases. Several JAK1 selective compounds are being investigated clinically to determine their anti-inflammatory potential. We used recombinant enzymes and primary human lymphocytes to assess the JAK1 specificity of itacitinib (INCB039110) and study inhibition of signal transducers and activators of transcription (STAT) signaling. Rodent models of arthritis and inflammatory bowel disease were subsequently explored to elucidate the efficacy of orally administered itacitinib on inflammatory pathogenesis. Itacitinib is a potent and selective JAK1 inhibitor when profiled against the other JAK family members. Upon oral administration in rodents, itacitinib achieved dose-dependent pharmacokinetic exposures that highly correlated with STAT3 pharmacodynamic pathway inhibition. Itacitinib ameliorated symptoms and pathology of established experimentally-induced arthritis in a dose-dependent manner. Furthermore, itacitinib effectively delayed disease onset, reduced symptom severity, and accelerated recovery in three distinct mouse models of inflammatory bowel disease. Low dose itacitinib administered via cannula directly into the colon was highly efficacious in TNBS-induced colitis but with minimal systemic drug exposure, suggesting localized JAK1 inhibition is sufficient for disease amelioration. Itacitinib treatment in an acute graft-versus-host disease (GvHD) model rapidly reduced inflammatory markers within lymphocytes and target tissue, resulting in a marked improvement in disease symptoms. This is the first manuscript describing itacitinib as a potent and selective JAK1 inhibitor with anti-inflammatory activity across multiple preclinical disease models. These data support the scientific rationale for ongoing clinical trials studying itacitinib in select GvHD patient populations.
MeSH term(s)	Animals ; Arthritis, Experimental/drug therapy ; Azetidines/pharmacokinetics ; Azetidines/pharmacology ; Azetidines/therapeutic use ; Chemokine CCL2/drug effects ; Colitis/chemically induced ; Colitis/drug therapy ; Dose-Response Relationship, Drug ; Graft vs Host Disease/drug therapy ; Humans ; Inflammation/drug therapy ; Inflammatory Bowel Diseases/drug therapy ; Isonicotinic Acids/pharmacokinetics ; Isonicotinic Acids/pharmacology ; Isonicotinic Acids/therapeutic use ; Janus Kinase 1/antagonists & inhibitors ; Lymphocytes/drug effects ; Mice ; Mice, Inbred BALB C ; Primary Cell Culture ; Rats ; Rats, Inbred Lew ; STAT Transcription Factors/drug effects ; STAT3 Transcription Factor/drug effects ; Signal Transduction/drug effects ; T-Lymphocytes/drug effects
Chemical Substances	Azetidines ; CCL2 protein, human ; Chemokine CCL2 ; INCB039110 ; Isonicotinic Acids ; STAT Transcription Factors ; STAT3 Transcription Factor ; STAT3 protein, human ; JAK1 protein, human (EC 2.7.10.2) ; Janus Kinase 1 (EC 2.7.10.2)
Language	English
Publishing date	2020-08-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2020.173505
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Zs.A 522: Show issues

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Article: Development of tendon structure and function: regulation of collagen fibrillogenesis.

Zhang, G / Young, B B / Ezura, Y / Favata, M / Soslowsky, L J / Chakravarti, S / Birk, D E

Journal of musculoskeletal & neuronal interactions

2005 Volume 5, Issue 1, Page(s) 5–21

Abstract: In the tendon, the development of mature mechanical properties is dependent on the assembly of a tendon-specific extracellular matrix. This matrix is synthesized by the tendon fibroblasts and composed of collagen fibrils organized as fibers, as well as ... ...

Abstract	In the tendon, the development of mature mechanical properties is dependent on the assembly of a tendon-specific extracellular matrix. This matrix is synthesized by the tendon fibroblasts and composed of collagen fibrils organized as fibers, as well as fibril-associated collagenous and non-collagenous proteins. All of these components are integrated, during development and growth, to form a functional tissue. During tendon development, collagen fibrillogenesis and matrix assembly progress through multiple steps where each step is regulated independently, culminating in a structurally and functionally mature tissue. Collagen fibrillogenesis occurs in a series of extracellular compartments where fibril intermediates are assembled and mature fibrils grow through a process of post-depositional fusion of the intermediates. Linear and lateral fibril growth occurs after the immature fibril intermediates are incorporated into fibers. The processes are regulated by interactions of extracellular macromolecules with the fibrils. Interactions with quantitatively minor fibrillar collagens, fibril-associated collagens and proteoglycans influence different steps in fibrillogenesis and the extracellular microdomains provide a mechanism for the tendon fibroblasts to regulate these extracellular interactions.
MeSH term(s)	Animals ; Collagen/biosynthesis ; Collagen/ultrastructure ; Extracellular Matrix/metabolism ; Extracellular Matrix/ultrastructure ; Fibril-Associated Collagens/metabolism ; Fibroblasts/metabolism ; Fibroblasts/ultrastructure ; Humans ; Macromolecular Substances/metabolism ; Proteoglycans/metabolism ; Tendons/growth & development ; Tendons/metabolism ; Tendons/ultrastructure
Chemical Substances	Fibril-Associated Collagens ; Macromolecular Substances ; Proteoglycans ; Collagen (9007-34-5)
Language	English
Publishing date	2005-03
Publishing country	Greece
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	2041366-X
ISSN	1108-7161
ISSN	1108-7161
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Zs.A 5401: Show issues

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Article: Variation of biomechanical, structural, and compositional properties along the tendon to bone insertion site.

Thomopoulos, Stavros / Williams, Gerald R / Gimbel, Jonathan A / Favata, Michele / Soslowsky, Louis J

Journal of orthopaedic research : official publication of the Orthopaedic Research Society

2003 Volume 21, Issue 3, Page(s) 413–419

Abstract: The tendon to bone insertion site is a complex transitional region that links two very different materials. The insertion site must transfer a complex loading environment effectively to prevent injury and provide proper joint function. In order to ... ...

Abstract	The tendon to bone insertion site is a complex transitional region that links two very different materials. The insertion site must transfer a complex loading environment effectively to prevent injury and provide proper joint function. In order to accomplish this load transfer effectively, the properties of the insertion site were hypothesized to vary along its length. The quasilinear viscoelastic (QLV) Model was used to determine biomechanical properties, polarized light analysis was used to quantitate collagen orientation (structure), and in situ hybridization was used to determine the expression of extracellular matrix genes (composition). All assays were performed at two insertion site locations: the tendon end of the insertion and the bony end of the insertion. Biomechanically, the apparent properties of peak strain, the coefficients (A and B) that describe the elastic component of the QLV model, and one of the coefficients (tau(1)) of the viscous component of the model were significantly higher, while another of the coefficients (C) of the viscous component was significantly lower at the tendon insertion compared to the bony insertion. The collagen was significantly more oriented at the tendon insertion compared to the bony insertion. Finally, collagen types II, IX, and X, and aggrecan were localized only to the bony insertion, while decorin and biglycan were localized only to the tendon insertion. Thus, the tendon to bony insertion site varies dramatically along its length in terms of its viscoelastic properties, collagen structure, and extracellular matrix composition.
MeSH term(s)	Aggrecans ; Animals ; Biomechanical Phenomena ; Collagen Type II/genetics ; Collagen Type IX/genetics ; Collagen Type X/genetics ; Elasticity ; Extracellular Matrix Proteins/genetics ; Humerus/physiology ; In Situ Hybridization ; Lectins, C-Type ; Models, Biological ; Proteoglycans/genetics ; RNA, Messenger/analysis ; Rats ; Rats, Sprague-Dawley ; Shoulder Joint/physiology ; Tendons/physiology
Chemical Substances	Agc1 protein, rat ; Aggrecans ; Collagen Type II ; Collagen Type IX ; Collagen Type X ; Extracellular Matrix Proteins ; Lectins, C-Type ; Proteoglycans ; RNA, Messenger
Language	English
Publishing date	2003-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	605542-4
ISSN	1554-527X ; 0736-0266
ISSN (online)	1554-527X
ISSN	0736-0266
DOI	10.1016/S0736-0266(03)00057-3
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Zs.A 1879: Show issues

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Article: The Novel Bromodomain and Extraterminal Domain Inhibitor INCB054329 Induces Vulnerabilities in Myeloma Cells That Inform Rational Combination Strategies.

Stubbs, Matthew C / Burn, Timothy C / Sparks, Richard / Maduskuie, Thomas / Diamond, Sharon / Rupar, Mark / Wen, Xiaoming / Volgina, Alla / Zolotarjova, Nina / Waeltz, Paul / Favata, Margaret / Jalluri, Ravi / Liu, Huiqing / Liu, Xuesong Mike / Li, Jun / Collins, Robert / Falahatpisheh, Nikoo / Polam, Padmaja / DiMatteo, Darlise /

Feldman, Patricia / Dostalik, Valerie / Thekkat, Pramod / Gardiner, Christine / He, Xin / Li, Yanlong / Covington, Maryanne / Wynn, Richard / Ruggeri, Bruce / Yeleswaram, Swamy / Xue, Chu-Biao / Yao, Wenqing / Combs, Andrew P / Huber, Reid / Hollis, Gregory / Scherle, Peggy / Liu, Phillip C C

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Volume 25, Issue 1, Page(s) 300–311

Abstract: Purpose: Bromodomain and extraterminal domain (BET) proteins regulate the expression of many cancer-associated genes and pathways; BET inhibitors have demonstrated activity in diverse models of hematologic and solid tumors. We report the preclinical ... ...

Abstract	Purpose: Bromodomain and extraterminal domain (BET) proteins regulate the expression of many cancer-associated genes and pathways; BET inhibitors have demonstrated activity in diverse models of hematologic and solid tumors. We report the preclinical characterization of INCB054329, a structurally distinct BET inhibitor that has been investigated in phase I clinical trials. Experimental design: We used multiple myeloma models to investigate vulnerabilities created by INCB054329 treatment that could inform rational combinations. Results: In addition to c-MYC, INCB054329 decreased expression of oncogenes Conclusions: Preclinical data reveal insights into vulnerabilities created in myeloma cells by BET protein inhibition and potential strategies that can be leveraged in clinical studies to enhance the activity of INCB054329.
MeSH term(s)	Animals ; Cell Cycle Proteins/antagonists & inhibitors ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Heterografts ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Janus Kinases/genetics ; Mice ; Multiple Myeloma/drug therapy ; Multiple Myeloma/genetics ; Multiple Myeloma/pathology ; Organic Chemicals/pharmacology ; Protein Binding/drug effects ; Proteins/antagonists & inhibitors ; Proteins/genetics ; Proto-Oncogene Proteins c-myc/genetics ; Receptor, Fibroblast Growth Factor, Type 3/genetics ; Receptors, Interleukin-6/genetics ; Repressor Proteins/genetics ; STAT3 Transcription Factor/genetics ; Signal Transduction/drug effects ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/genetics
Chemical Substances	BRD4 protein, human ; Cell Cycle Proteins ; IL6R protein, human ; INCB054329 ; MYC protein, human ; Organic Chemicals ; Proteins ; Proto-Oncogene Proteins c-myc ; Receptors, Interleukin-6 ; Repressor Proteins ; STAT3 Transcription Factor ; Transcription Factors ; bromodomain and extra-terminal domain protein, human ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; NSD2 protein, human (EC 2.1.1.43) ; FGFR3 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 3 (EC 2.7.10.1) ; Janus Kinases (EC 2.7.10.2)
Language	English
Publishing date	2018-09-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-18-0098
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Zs.A 4223: Show issues

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Article ; Online: Comparative treatment of alpha-amanitin poisoning with N-acetylcysteine, benzylpenicillin, cimetidine, thioctic acid, and silybin in a murine model.

Tong, Tri C / Hernandez, Mark / Richardson, William H / Betten, David P / Favata, Michael / Riffenburgh, Robert H / Clark, Richard F / Tanen, David A

Annals of emergency medicine

2007 Volume 50, Issue 3, Page(s) 282–288

Abstract: Study objective: The foraging of wild mushrooms can be complicated by toxicity from several mushroom types. Amatoxin, a peptide contained in several mushroom species, accounts for the majority of severe mushroom poisonings by binding to RNA polymerase ... ...

Abstract	Study objective: The foraging of wild mushrooms can be complicated by toxicity from several mushroom types. Amatoxin, a peptide contained in several mushroom species, accounts for the majority of severe mushroom poisonings by binding to RNA polymerase II irreversibly, leading to severe hepatonecrosis. There is no effective antidote for severe amatoxin poisoning. We compare the effectiveness of 5 potential antidotal therapies in limiting the degree of hepatonecrosis in a randomized, controlled, murine model of amatoxin-induced hepatotoxicity. Methods: One hundred eighty male Institute of Cancer Research mice were randomized into 6 equal groups. Within each group, 21 mice were intraperitoneally injected with 0.6 mg/kg of alpha-amanitin (amatoxin); the remaining 9 were injected with 0.9% normal saline solution. Four hours postinjection, each group of 30 mice was randomized to 1 of 5 intraperitoneal treatments (N-acetylcysteine, benzylpenicillin, cimetidine, thioctic acid, or silybin) or normal saline solution. Repeated dosing was administered intraperitoneally every 4 to 6 hours for 48 hours. After 48 hours of treatment, each subject was killed, cardiac blood was aspirated for hepatic aminotransferase measurements (alanine transaminase and aspartate transaminase), and liver specimens were harvested to evaluate the extent of hepatonecrosis. The degree of hepatonecrosis was determined by a pathologist blinded to the treatment group and divided into 5 categories according to percentage of hepatonecrosis. Results: Amanitin significantly increased aspartate transaminase in treated mice compared with normal saline solution-treated controls (mean [SD] 2,441 [2,818] IU/L versus 310 [252]; P=.03). None of the antidotal therapies were found to significantly decrease the increase in aminotransferases compared with controls. Further, none of the antidotal therapies demonstrated an important decrease in hepatonecrosis compared with controls when a histologic grading scale was used. Conclusion: In this murine model, N-acetylcysteine, benzylpenicillin, cimetidine, thioctic acid, and silybin were not effective in limiting hepatic injury after alpha-amanitin poisoning. Increases of aminotransferases and degrees of histologic hepatonecrosis were not attenuated by these antidotal therapies.
MeSH term(s)	Acetylcysteine/administration & dosage ; Acetylcysteine/pharmacology ; Alanine Transaminase/blood ; Amanitins/poisoning ; Animals ; Antidotes/administration & dosage ; Antidotes/pharmacology ; Aspartate Aminotransferases/blood ; Chemical and Drug Induced Liver Injury/drug therapy ; Cimetidine/administration & dosage ; Cimetidine/pharmacology ; Disease Models, Animal ; Male ; Mice ; Mushroom Poisoning/drug therapy ; Penicillin G/administration & dosage ; Penicillin G/pharmacology ; Random Allocation ; Silymarin/administration & dosage ; Silymarin/pharmacology ; Thioctic Acid/administration & dosage ; Thioctic Acid/pharmacology
Chemical Substances	Amanitins ; Antidotes ; Silymarin ; silybin (4RKY41TBTF) ; amatoxin (58250-15-0) ; Thioctic Acid (73Y7P0K73Y) ; Cimetidine (80061L1WGD) ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Penicillin G (Q42T66VG0C) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2007-09
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603080-4
ISSN	1097-6760 ; 0196-0644
ISSN (online)	1097-6760
ISSN	0196-0644
DOI	10.1016/j.annemergmed.2006.12.015
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Zs.A 1344: Show issues

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Article: Regenerative properties of fetal sheep tendon are not adversely affected by transplantation into an adult environment.

Favata, Michele / Beredjiklian, Pedro K / Zgonis, Miltiadis H / Beason, David P / Crombleholme, Timothy M / Jawad, Abbas F / Soslowsky, Louis J

Journal of orthopaedic research : official publication of the Orthopaedic Research Society

2006 Volume 24, Issue 11, Page(s) 2124–2132

Abstract: Tendon injuries account for a significant number of musculoskeletal afflictions each year. While new surgical techniques and rehabilitation protocols have led to improved clinical outcomes, postsurgical scarring remains the most problematic aspect of ... ...

Abstract	Tendon injuries account for a significant number of musculoskeletal afflictions each year. While new surgical techniques and rehabilitation protocols have led to improved clinical outcomes, postsurgical scarring remains the most problematic aspect of tendon repair. In contrast to this typical pattern of fibrosis, recent studies have shown that fetal tendon is capable of healing without scar. However, whether this regenerative healing pattern is intrinsic to the fetal tissue itself or the result of its environment is not known. Thus, the objective of this study is to examine the influence of an adult environment on healing in adult and fetal tendons. We hypothesized that injured fetal tendon tissue transplanted into an adult environment would retain a regenerative healing pattern after injury, demonstrating normal histological and mechanical properties. Our results support this hypothesis. Histological analyses revealed considerable alterations in adult tendon transplants after injury while fetal transplants showed no abnormalities. The injured adult tendons also demonstrated elevated levels of TGF-beta1, bFGF, and CD44 at the wound site, whereas the fetal specimens showed little or no such changes in response to injury. The data from our biomechanical studies further corroborate these observations, with significant decreases in the stiffness, modulus, and almost all viscoelastic properties in wounded versus unwounded adult tendons, and fetal specimens showing no differences in mechanical properties between the wounded and unwounded groups. Thus, the results of our investigation demonstrate that the adult environment is not an impediment to scarless repair and that this capability is intrinsic to the fetal tendon itself. Our study also begins to provide insight into the mechanisms controlling this regenerative response.
MeSH term(s)	Age Factors ; Animals ; Biomarkers/metabolism ; Cicatrix/metabolism ; Cicatrix/pathology ; Fetal Tissue Transplantation ; Fetus/physiology ; Fibroblast Growth Factor 2/metabolism ; Hyaluronan Receptors/metabolism ; Models, Animal ; Pliability ; Regeneration/physiology ; Sheep ; Tendon Injuries/embryology ; Tendon Injuries/surgery ; Tendons/metabolism ; Tendons/physiology ; Tendons/transplantation ; Transforming Growth Factor beta1/metabolism ; Wound Healing/physiology
Chemical Substances	Biomarkers ; Hyaluronan Receptors ; Transforming Growth Factor beta1 ; Fibroblast Growth Factor 2 (103107-01-3)
Language	English
Publishing date	2006-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605542-4
ISSN	1554-527X ; 0736-0266
ISSN (online)	1554-527X
ISSN	0736-0266
DOI	10.1002/jor.20271
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Zs.A 1879: Show issues

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Article ; Online: INCB040093 Is a Novel PI3K

Shin, Niu / Li, Yun-Long / Mei, Song / Wang, Kathy He / Hall, Leslie / Katiyar, Kamna / Wang, Qian / Yang, Gengjie / Rumberger, Beth / Leffet, Lynn / He, Xin / Rupar, Mark / Bowman, Kevin / Favata, Margaret / Li, Jun / Liu, Mike / Li, Yanlong / Covington, Maryanne / Koblish, Holly /

Soloviev, Maxim / Shuey, Dana / Burn, Timothy / Diamond, Sharon / Fridman, Jordan / Combs, Andrew / Yao, Wenqing / Yeleswaram, Swamy / Hollis, Gregory / Vaddi, Kris / Huber, Reid / Newton, Robert / Scherle, Peggy

The Journal of pharmacology and experimental therapeutics

2017 Volume 364, Issue 1, Page(s) 120–130

Abstract: Phosphatidylinositol 3-kinase delta ( ... ...

Abstract	Phosphatidylinositol 3-kinase delta (PI3K
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; B-Lymphocytes/drug effects ; B-Lymphocytes/metabolism ; Cell Line ; Cell Proliferation/drug effects ; Chemokine CCL4/metabolism ; Dogs ; Female ; Humans ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/metabolism ; Lymphoma, Non-Hodgkin/drug therapy ; Lymphoma, Non-Hodgkin/metabolism ; Male ; Mice ; Mice, SCID ; Monocytes/drug effects ; Monocytes/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neutrophils/drug effects ; Neutrophils/metabolism ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Protein Kinase Inhibitors/pharmacology ; Rats ; T-Lymphocytes/drug effects ; T-Lymphocytes/metabolism
Chemical Substances	Antineoplastic Agents ; Chemokine CCL4 ; Protein Kinase Inhibitors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2017-11-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.117.244947
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