Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Under Re-organization)
Formerly: Current Medicinal Chemistry - Immunology, Endocrine and Metabolic Agents
Volume 18, 2 Issues, 2018
ISSN: 1875-6115 (Online)
ISSN: 1875-5222 (Print)
This journal supports open access
ISSN: 1875-6115 (Online)
ISSN: 1875-5222 (Print)
This journal supports open access
Contents
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry, Volume 16 - Number 3
Editorial
Review Article
Obesity: An Emerging Importance of Progenitors
, 16(3): 148 - 160Drenka Trivanović, Jelena Krstić, Juan Francisco Santibanez, Aleksandra Jauković and Diana Bugarski
DOI: 10.2174/1871522217666170105092757
Obesity: An Emerging Importance of Progenitors
Research Article
Angiotensin-II, a Potent Peptide, Participates in the Development of Hepatic Dysfunctions
, 16(3): 161 - 177Muhammad A.T. Sagor, Muhammad M. Mohib, Muhammad S. Azam, Anisur Rahman, Foysal T. Tanmoy, Wahida K. Chowdhury, Nafees Uddin Chowdhury, Hasan M. Reza and Muhammad A. Alam
DOI: 10.2174/1871522217666170106103001
Angiotensin-II, a Potent Peptide, Participates in the Development of Hepatic Dysfunctions
Research Article
VIP Signaling Fails to Alter Gene Expression but Induces Different [cAMP]i Responses in Human Malignant Hut-78 and Molt-4 T Cell Lines; Implications for Different G-protein Coupling for VIP Receptors
, 16(3): 178 - 198Travis V.-D. Steen, Manpreet Bains, Steve Wanjara, Brittany Bisnett, Caleb Laney, Ben Huber, Sheri T. Dorsam, Jane M. Schuh and Glenn P. Dorsam
DOI: 10.2174/1871522217666170206152357
VIP Signaling Fails to Alter Gene Expression but Induces Different [cAMP]i Responses in Human Malignant Hut-78 and Molt-4 T Cell Lines; Implications for Different G-protein Coupling for VIP Receptors
Research Article
Silencing the Transcription Factor FOSL1 in Hyperproliferative HaCaT Cells Makes Them Susceptible to IFN-γ
, 16(3): 199 - 209Prelovskaya Anna, Mezentsev Alexandre, Piruzian Eleonora, Soboleva Anna and Bruskin Sergey
DOI: 10.2174/1871522216666161111115903
Silencing the Transcription Factor FOSL1 in Hyperproliferative HaCaT Cells Makes Them Susceptible to IFN-γ
Acknowledgement
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