Example of Current Signal Transduction Therapy format
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Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format
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Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format Example of Current Signal Transduction Therapy format
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open access Open Access ISSN: 15743624

Current Signal Transduction Therapy — Template for authors

Publisher: Bentham Science
Categories Rank Trend in last 3 yrs
Pharmacology (medical) #157 of 246 up up by 43 ranks
Endocrinology #103 of 117 up up by 9 ranks
journal-quality-icon Journal quality:
Medium
calendar-icon Last 4 years overview: 72 Published Papers | 116 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 03/06/2020
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Journal Performance & Insights

  • CiteRatio
  • SJR
  • SNIP

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

1.6

33% from 2019

CiteRatio for Current Signal Transduction Therapy from 2016 - 2020
Year Value
2020 1.6
2019 1.2
2018 0.6
2017 0.3
2016 0.9
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 33% 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.

0.128

10% from 2019

SJR for Current Signal Transduction Therapy from 2016 - 2020
Year Value
2020 0.128
2019 0.142
2018 0.138
2017 0.129
2016 0.232
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 10% 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.

0.466

121% from 2019

SNIP for Current Signal Transduction Therapy from 2016 - 2020
Year Value
2020 0.466
2019 0.211
2018 0.132
2017 0.096
2016 0.112
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has increased by 121% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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CiteRatio: 6.3 | SJR: 1.196 | SNIP: 1.603

Current Signal Transduction Therapy

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Bentham Science

Current Signal Transduction Therapy

In recent years a breakthrough has occurred in our understanding of the molecular pathomechanisms of human diseases whereby most of our diseases are related to intra and intercellular communication disorders. The concept of signal transduction therapy has got into the front li...... Read More

Pharmacology (medical)

Endocrinology

Medicine

i
Last updated on
02 Jun 2020
i
ISSN
1574-3624
i
Impact Factor
Low - 0.165
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Yellow faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
Vancouver
i
Citation Type
Numbered
[25]
i
Bibliography Example
Blonder, G E, Tinkham, M, & Klapwijk, T M. Transition from metallic to tunnel- ing regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B. 2013;87(10):100510.

Top papers written in this journal

Journal Article DOI: 10.2174/157436206775269235
Nuclear Factor-κB: A Holy Grail in Cancer Prevention and Therapy

Abstract:

Nuclear factor-� B (NF-� B) is a transcription factor that is activated in response to various inflammatory stimuli such as cytokines, growth factors, hormones, mitogens, carcinogens, chemotherapeutic agents, viral products, eukaryotic parasites, endotoxin, fatty acids, metals, radiation, hypoxia, and psychological, physical,... Nuclear factor-� B (NF-� B) is a transcription factor that is activated in response to various inflammatory stimuli such as cytokines, growth factors, hormones, mitogens, carcinogens, chemotherapeutic agents, viral products, eukaryotic parasites, endotoxin, fatty acids, metals, radiation, hypoxia, and psychological, physical, oxidative, and chemical stresses. In addition, constitutively active NF-�B is frequently encountered in a wide variety of tumors, including breast, ovarian, colon, pancreatic, thyroid, prostate, lung, head and neck, bladder, and skin cancers; B-cell lymphoma; Hodgkin's disease; T-cell lymphoma; adult T-cell leukemia; acute lymphoblastic leukemia; multiple myeloma; chronic lymphocytic leukemia; and acute myelogenous leukemia. Furthermore, NF-�B activation has been shown to regulate the expression of over 400 genes involved in cellular transformation, proliferation, inflammation, viral replication, antiapoptosis, angiogenesis, invasion and metastasis, oxidative stress, and osteoclastogenesis. Therefore, because of the critical role NF- �B plays in the pathogenesis of cancer, specific inhibitors of this factor are being sought. Agents that prevent cancer or inflammation have been found to suppress NF-� B activation. Although IBkinase is the major kinase, over 30 different protein kinases have been linked to the activation of NF-�B by different stimuli. The development of a drug that can specifically suppress NF-�B activation requires a full understanding of the mechanism by which NF-�B is activated in response to these various stimuli. read more read less

Topics:

Cancer (58%)58% related to the paper, Chronic lymphocytic leukemia (57%)57% related to the paper, Leukemia (56%)56% related to the paper, Metastasis (54%)54% related to the paper, Kinase (52%)52% related to the paper
View PDF
65 Citations
open accessOpen access Journal Article DOI: 10.2174/1574362409666140206223014
Mechanisms of Acquired Resistance to Tyrosine Kinase Inhibitors in Clear - Cell Renal Cell Carcinoma (ccRCC)
Zofia F. Bielecka1, Anna M. Czarnecka, Wojciech Solarek1, Anna Kornakiewicz1, Cezary Szczylik

Abstract:

Researchers have specified different subsets of tyrosine kinase inhibitors potential resistance mechanisms in clear-cell renal cell carcinoma. In most papers published until now, drug resistance is divided into intrinsic and acquired, and typically multi-drug resistance (MDR) protein is described. Herein, the authors focus on... Researchers have specified different subsets of tyrosine kinase inhibitors potential resistance mechanisms in clear-cell renal cell carcinoma. In most papers published until now, drug resistance is divided into intrinsic and acquired, and typically multi-drug resistance (MDR) protein is described. Herein, the authors focus on molecular analysis concerning acquired, non-genetic resistance to TKIs, with insight into specific biological processes. read more read less

Topics:

Clear cell renal cell carcinoma (59%)59% related to the paper, Axitinib (55%)55% related to the paper, Sunitinib (55%)55% related to the paper, Tyrosine kinase (52%)52% related to the paper, Drug resistance (52%)52% related to the paper
59 Citations
Journal Article DOI: 10.2174/157436207781745300
Fluoride Interactions: From Molecules to Disease

Abstract:

Fluoride has long been known to influence the activity of various enzymes in vitro. Later it has been demonstrated that many effects primarily attributed to fluoride are caused by synergistic action of fluoride plus aluminum. Aluminofluoride complexes have been widely used as analogues of phosphate groups to study phosphoryl ... Fluoride has long been known to influence the activity of various enzymes in vitro. Later it has been demonstrated that many effects primarily attributed to fluoride are caused by synergistic action of fluoride plus aluminum. Aluminofluoride complexes have been widely used as analogues of phosphate groups to study phosphoryl transfer reactions and heterotrimeric G proteins involvement. A num- ber of reports on their use have appeared, with far-reaching consequences for our understanding of fundamental biological processes. Fluoride plus aluminum send false messages, which are amplified by processes of signal transduction. Many investigations of the long- term administration of fluoride to laboratory animals have demonstrated that fluoride and aluminofluoride complexes can elicit impair- ment of homeostasis, growth, development, cognition, and behavior. Ameliorative effects of calcium, vitamins C, D, and E have been re- ported. Numerous epidemiological, ecological, and clinical studies have shown the effects of fluoride on humans. Millions of people live in endemic fluorosis areas. A review of fluoride interactions from molecules to disease is necessary for a sound scientific assessment of health risks, which may be linked to the chronic intake of small doses of fluoride and aluminum from environmental and artificial sources. read more read less

Topics:

Fluoride (65%)65% related to the paper
View PDF
58 Citations
open accessOpen access Journal Article DOI: 10.2174/1574362409666140206221931
Resistance of Cancer Cells to Targeted Therapies Through the Activation of Compensating Signaling Loops

Abstract:

The emergence of low molecular weight kinase inhibitors as “targeted” drugs has led to remarkable advances in the treatment of cancer patients. The clinical benefits of these tumor therapies, however, vary widely in patient populations and with duration of treatment. Intrinsic and acquired resistance against such drugs limits... The emergence of low molecular weight kinase inhibitors as “targeted” drugs has led to remarkable advances in the treatment of cancer patients. The clinical benefits of these tumor therapies, however, vary widely in patient populations and with duration of treatment. Intrinsic and acquired resistance against such drugs limits their efficacy. In addition to the well studied mechanisms of resistance based upon drug transport and metabolism, genetic alterations in drug target structures and the activation of compensatory cell signaling have received recent attention. Adaptive responses can be triggered which counteract the initial dependence of tumor cells upon a particular signaling molecule and allow only a transient inhibition of tumor cell growth. These compensating signaling mechanisms are often based upon the relief of repression of regulatory feedback loops. They might involve cell autonomous, intracellular events or they can be mediated via the secretion of growth factor receptor ligands into the tumor microenvironment and signal induction in an auto- or paracrine fashion. The transcription factors Stat3 and Stat5 mediate the biological functions of cytokines, interleukins and growth factors and can be considered as endpoints of multiple signaling pathways. In normal cells this activation is transient and the Stat molecules return to their non-phosphorylated state within a short time period. In tumor cells the balance between activating and de-activating signals is disturbed resulting in the persistent activation of Stat3 or Stat5. The constant activation of Stat3 induces the expression of target genes, which cause the proliferation and survival of cancer cells, as well as their migration and invasive behavior. Activating components of the Jak-Stat pathway have been recognized as potentially valuable drug targets and important principles of compensatory signaling circuit induction during targeted drug treatment have been discovered in the context of kinase inhibition studies in HNSCC cells [1]. The treatment of HNSCC with a specific inhibitor of c-Src, initially resulted in reduced Stat3 and Stat5 activation and subsequently an arrest of cell proliferation and increased apoptosis. However, the inhibition of c-Src only caused a persistent inhibition of Stat5, whereas the inhibition of Stat3 was only transient. The activation of Stat3 was restored within a short time period in the presence of the c-Src inhibitor. This process is mediated through the suppression of P-Stat5 activity and the decrease in the expression of the Stat5 dependent target gene SOCS2, a negative regulator of Jak2. Jak2 activity is enhanced upon SOCS2 downregulation and causes the reactivation of Stat3. A similar observation has been made upon inhibition of Bmx, bone marrow kinase x-linked, activated in the murine glioma cell lines Tu-2449 and Tu-9648. Its inhibition resulted in a transient decrease of P-Stat3 and the induction of a compensatory Stat3 activation mechanism, possibly through the relief of negative feedback inhibition and Jak2 activation. These observations indicate that the inhibition of a single tyrosine kinase might not be sufficient to induce lasting therapeutic effects in cancer patients. Compensatory kinases and pathways might become activated and maintain the growth and survival of tumor cells. The definition of these escape pathways and their preemptive inhibition will suggest effective new combination therapies for cancer. read more read less

Topics:

Growth factor receptor (57%)57% related to the paper, Signal Induction (56%)56% related to the paper, Cell signaling (56%)56% related to the paper, Tumor microenvironment (56%)56% related to the paper, Signal transduction (56%)56% related to the paper
57 Citations
Journal Article DOI: 10.2174/157436209789057467
Targeting JAK/STAT Signaling Pathway in Inflammatory Diseases

Topics:

Janus kinase (61%)61% related to the paper, JAK-STAT signaling pathway (59%)59% related to the paper
57 Citations
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Current Signal Transduction Therapy format uses Vancouver citation style.

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Sure. We support all the top citation styles like APA style, MLA style, Vancouver style, Harvard style, Chicago style, etc. For example, in case of this journal, when you write your paper and hit autoformat, it will automatically update your article as per the Current Signal Transduction Therapy citation style.

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One little Google search can get you the Word template for any journal. However, why do you need a Word template when you can write your entire manuscript on SciSpace, autoformat it as per Current Signal Transduction Therapy's guidelines and download the same in Word, PDF and LaTeX formats? Try us out!.

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To be honest, the answer is NO. The impact factor is one of the many elements that determine the quality of a journal. Few of those factors the review board, rejection rates, frequency of inclusion in indexes, Eigenfactor, etc. You must assess all the factors and then take the final call.

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:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

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S. No. Citation Style Type
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2. Numbered
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4. Author Year (Cited Pages)
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SciSpace would allow download of your references in Current Signal Transduction Therapy Endnote style, according to bentham-science guidelines.

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