Example of Expert Opinion on Therapeutic Targets format
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Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format
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Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format Example of Expert Opinion on Therapeutic Targets format
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open access Open Access ISSN: 14728222 e-ISSN: 17447631
recommended Recommended

Expert Opinion on Therapeutic Targets — Template for authors

Publisher: Taylor and Francis
Categories Rank Trend in last 3 yrs
Clinical Biochemistry #10 of 113 up up by 3 ranks
Pharmacology #32 of 297 down down by 2 ranks
Drug Discovery #18 of 145 down down by 6 ranks
Molecular Medicine #26 of 167 up up by 4 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 333 Published Papers | 2992 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 12/06/2020
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FAQ

Journal Performance & Insights

  • Impact Factor
  • CiteRatio
  • SJR
  • SNIP

Impact factor determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

5.473

18% from 2018

Impact factor for Expert Opinion on Therapeutic Targets from 2016 - 2019
Year Value
2019 5.473
2018 4.621
2017 4.598
2016 4.873
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 18% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

CiteRatio is a measure of average citations received per peer-reviewed paper published in the journal.

9.0

6% from 2019

CiteRatio for Expert Opinion on Therapeutic Targets from 2016 - 2020
Year Value
2020 9.0
2019 8.5
2018 8.4
2017 7.9
2016 7.8
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 6% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR) measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

1.964

16% from 2019

SJR for Expert Opinion on Therapeutic Targets from 2016 - 2020
Year Value
2020 1.964
2019 1.699
2018 1.47
2017 1.597
2016 1.765
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 16% in last years.
  • This journal’s SJR is in the top 10 percentile category.

Source Normalized Impact per Paper (SNIP) measures actual citations received relative to citations expected for the journal's category.

1.376

12% from 2019

SNIP for Expert Opinion on Therapeutic Targets from 2016 - 2020
Year Value
2020 1.376
2019 1.229
2018 1.073
2017 1.014
2016 1.11
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has increased by 12% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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Expert Opinion on Therapeutic Targets

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Taylor and Francis

Expert Opinion on Therapeutic Targets

Expert Opinion on Therapeutic Targets ranks #39 of 260 in the Pharmacology & Pharmacy category in the 2011 ISI Journal Citation Reports. Expert Opinion on Therapeutic Targets (ISSN 1472-8222 [print], 1744-7631 [electronic]) is a MEDLINE-indexed, peer-reviewed, international jo...... Read More

Clinical Biochemistry

Pharmacology

Drug Discovery

Molecular Medicine

Biochemistry, Genetics and Molecular Biology

i
Last updated on
12 Jun 2020
i
ISSN
1472-8222
i
Impact Factor
High - 1.206
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
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Bibliography Name
Taylor and Francis Custom Citation
i
Citation Type
Numbered
[25]
i
Bibliography Example
Blonder GE, Tinkham M, Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys Rev B. 1982; 25(7):4515–4532. Available from: 10.1103/PhysRevB.25.4515.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1517/14728222.2011.645805
Targeting the MAPK–RAS–RAF signaling pathway in cancer therapy
Libero Santarpia1, Scott M. Lippman1, Adel K. El-Naggar1

Abstract:

Introduction: The MAPK pathway comprises several key signaling components and phosphorylation events that play a role in tumorigenesis. These activated kinases transmit extracellular signals that regulate cell growth, differentiation, proliferation, apoptosis and migration functions. Alteration of the RAS–RAF–MEK–ERK–MAPK (RA... Introduction: The MAPK pathway comprises several key signaling components and phosphorylation events that play a role in tumorigenesis. These activated kinases transmit extracellular signals that regulate cell growth, differentiation, proliferation, apoptosis and migration functions. Alteration of the RAS–RAF–MEK–ERK–MAPK (RAS–MAPK) pathway has been reported in human cancer as a result of abnormal activation of receptor tyrosine kinases or gain-of-function mutations mainly in the RAS or RAF genes. These pathways are considered potential therapeutic targets for cancer treatment. Recently, several small-molecule inhibitors targeting this pathway have been developed and are currently being tested in clinical trials. Areas covered: The biological role of the RAS–MAPK pathway, the consequence of its disregulation and the development of small-molecule inhibitors. The rationale for targeting the RAS–MAPK pathway and the application and the results of various inhibitory molecules as anticancer agents in clinical ... read more read less

Topics:

MAPK/ERK pathway (61%)61% related to the paper, JAK-STAT signaling pathway (59%)59% related to the paper, Mitogen-activated protein kinase (57%)57% related to the paper, c-Raf (56%)56% related to the paper, Receptor tyrosine kinase (54%)54% related to the paper
572 Citations
open accessOpen access Journal Article DOI: 10.1517/14728222.2011.648617
Targeting the EGFR signaling pathway in cancer therapy

Abstract:

Introduction: Cancer is a devastating disease; however, several therapeutic advances have recently been made, wherein EGFR and its family members have emerged as useful biomarkers and therapeutic targets. EGFR, a transmembrane glycoprotein is a member of the ERBB receptor tyrosine kinase superfamily. EGFR binds to its cognate... Introduction: Cancer is a devastating disease; however, several therapeutic advances have recently been made, wherein EGFR and its family members have emerged as useful biomarkers and therapeutic targets. EGFR, a transmembrane glycoprotein is a member of the ERBB receptor tyrosine kinase superfamily. EGFR binds to its cognate ligand EGF, which further induces tyrosine phosphorylation and receptor dimerization with other family members leading to enhanced uncontrolled proliferation. Several anti-EGFR therapies such as monoclonal antibodies and tyrosine kinase inhibitors have been developed, which has enabled clinicians to identify and treat specific patient cohorts. Areas covered: This review covers the basic mechanism of EGFR activation and the role of EGFR signaling in cancer progression. Furthermore, current developments made toward targeting the EGFR signaling pathway for the treatment of epithelial cancers and a summary of the various anti-EGFR therapeutic agents that are currently in use are also pre... read more read less

Topics:

Cyclin-dependent kinase 8 (60%)60% related to the paper, Receptor tyrosine kinase (59%)59% related to the paper, EGFR inhibitors (59%)59% related to the paper, ErbB (58%)58% related to the paper, Tyrosine phosphorylation (55%)55% related to the paper
567 Citations
Journal Article DOI: 10.1517/14728222.2011.639361
The RAS/RAF/MEK/ERK and the PI3K/AKT signalling pathways: role in cancer pathogenesis and implications for therapeutic approaches.

Abstract:

Introduction: The RAS/RAF/MAP kinase–ERK kinase (MEK)/extracellular-signal-regulated kinase (ERK) (MAPK) and the PI3K/AKT/mammalian target of rapamycin (mTOR) (PI3K) pathways are frequently deregulated in human cancer as a result of genetic alterations in their components or upstream activation of cell-surface receptors. Thes... Introduction: The RAS/RAF/MAP kinase–ERK kinase (MEK)/extracellular-signal-regulated kinase (ERK) (MAPK) and the PI3K/AKT/mammalian target of rapamycin (mTOR) (PI3K) pathways are frequently deregulated in human cancer as a result of genetic alterations in their components or upstream activation of cell-surface receptors. These signalling cascades are regulated by complex feedback and cross-talk mechanisms. Areas covered: In this review the key components of the MAPK and AKT pathways and their molecular alterations are described. The complex interactions between these signalling cascades are also analysed. Expert opinion: The observation that the MAPK and the PI3K pathways are often deregulated in human cancer makes the components of these signalling cascades interesting targets for therapeutic intervention. Recently, the presence of compensatory loops that activate one pathway following the blockade of the other signalling cascade has been demonstrated. Therefore, the blockade of both pathways with combin... read more read less

Topics:

Anti-apoptotic Ras signalling cascade (65%)65% related to the paper, MAPK/ERK pathway (61%)61% related to the paper, PI3K/AKT/mTOR pathway (56%)56% related to the paper, Protein kinase B (55%)55% related to the paper, Kinase (52%)52% related to the paper
542 Citations
open accessOpen access Journal Article DOI: 10.1517/14728222.11.11.1473
Targeting selectins and selectin ligands in inflammation and cancer
Steven R. Barthel1, Jacyln D Gavino, Leyla Descheny, Charles J. Dimitroff

Abstract:

Inflammation and cancer metastasis are associated with extravasation of leukocytes or tumor cells from blood into tissue. Such movement is believed to follow a coordinated and sequential molecular cascade initiated, in part, by the three members of the selectin family of carbohydrate-binding proteins: E-selectin (CD62E), L-se... Inflammation and cancer metastasis are associated with extravasation of leukocytes or tumor cells from blood into tissue. Such movement is believed to follow a coordinated and sequential molecular cascade initiated, in part, by the three members of the selectin family of carbohydrate-binding proteins: E-selectin (CD62E), L-selectin (CD62L) and P-selectin (CD62P). E-selectin is particularly noteworthy in disease by virtue of its expression on activated endothelium and on bone-skin microvascular linings and for its role in cell rolling, cell signaling and chemotaxis. E-selectin, along with L- or P-selectin, mediates cell tethering and rolling interactions through the recognition of sialo-fucosylated Lewis carbohydrates expressed on structurally diverse protein-lipid ligands on circulating leukocytes or tumor cells. Major advances in understanding the role of E-selectin in inflammation and cancer have been advanced by experiments assaying E-selectin-mediated rolling of leukocytes and tumor cells under hydrodynamic shear flow, by clinical models of E-selectin-dependent inflammation, by mice deficient in E-selectin and by mice deficient in glycosyltransferases that regulate the binding activity of E-selectin ligands. Here, the authors elaborate on how E-selectin and its ligands may facilitate leukocyte or tumor cell recruitment in inflammatory and metastatic settings. Antagonists that target cellular interactions with E-selectin and other members of the selectin family, including neutralizing monoclonal antibodies, competitive ligand inhibitors or metabolic carbohydrate mimetics, exemplify a growing arsenal of potentially effective therapeutics in controlling inflammation and the metastatic behavior of cancer. read more read less

Topics:

Selectin (57%)57% related to the paper, Inflammation (55%)55% related to the paper, Extravasation (53%)53% related to the paper, Cell signaling (51%)51% related to the paper, Metastasis (51%)51% related to the paper
333 Citations
Journal Article DOI: 10.1517/14728222.11.5.613
The IL-6/sIL-6R complex as a novel target for therapeutic approaches.
Stefan Rose-John1, Georg H. Waetzig, Jürgen Scheller1, Joachim Grötzinger1, Dirk Seegert

Abstract:

IL-6 plays a pivotal role in immune responses and certain oncologic conditions. The intense investigation of its biological activity and function led to the discovery of two different IL-6-driven signalling pathways. Binding to the membrane-bound IL-6 receptor (mIL-6R, CD126) causes the recruitment of two gp130 co-receptor mo... IL-6 plays a pivotal role in immune responses and certain oncologic conditions. The intense investigation of its biological activity and function led to the discovery of two different IL-6-driven signalling pathways. Binding to the membrane-bound IL-6 receptor (mIL-6R, CD126) causes the recruitment of two gp130 co-receptor molecules (CD130) and the activation of intracellular signalling cascades via gp130. Although this classical pathway is mainly limited to hepatocytes, neutrophils, monocytes/macrophages and certain other leukocyte populations, which express IL-6R on their surface, an alternative mechanism has also been described. Proteolytic cleavage of the mIL-6R protein or translation from alternatively spliced mRNA leads to the generation of a soluble form of the IL-6R (sIL-6R), which is likewise able to bind to IL-6. The resulting IL-6/sIL-6R complex is also capable of binding to gp130 and inducing intracellular signalling. Through this so-called 'trans-signalling' mechanism, IL-6 is able to stimulate cells that lack an endogenous mIL-6R. High levels of IL-6 and sIL-6R have been reported in several chronic inflammatory and autoimmune diseases as well as in cancer. Preclinical animal disease models have provided strong evidence that specific blockade of IL-6-regulated signalling pathways represents a promising approach for the therapy of these diseases. An optimised variant of the recently described fusion protein sgp30Fc is now heading towards its clinical evaluation. read more read less

Topics:

Cytokine (53%)53% related to the paper, Classical complement pathway (53%)53% related to the paper, Fusion protein (51%)51% related to the paper
324 Citations
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SHERPA/RoMEO Database

We have extracted this data from Sherpa Romeo to help our researchers understand the access level of this journal. The following table indicates the level of access a journal has as per Sherpa Romeo Archiving Policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
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  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

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