Muthu K. Shanmugam
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View article: Bioresponsive engineered nanoparticles for immunomodulation
Bioresponsive engineered nanoparticles for immunomodulation Open
Nanomaterials possess significant immunomodulatory capabilities, enhancing both disease prevention and therapeutic efficacy in vivo, yet their clinical translation is hindered by complex fabrication methods and high production costs. Futur…
View article: Omeprazole and cardiovascular risk via induction of statin dysmetabolism
Omeprazole and cardiovascular risk via induction of statin dysmetabolism Open
Background Statins are a first line treatment for reducing cardiovascular risk. While drug-drug interactions which cause symptomatic side effects are well known, drug- drug interactions which decrease statin effectiveness are poorly unders…
View article: Asparagine Synthetase Marks a Distinct Dependency Threshold for Cardiomyocyte Dedifferentiation
Asparagine Synthetase Marks a Distinct Dependency Threshold for Cardiomyocyte Dedifferentiation Open
BACKGROUND: Adult mammalian cardiomyocytes have limited proliferative capacity, but in specifically induced contexts they traverse through cell-cycle reentry, offering the potential for heart regeneration. Endogenous cardiomyocyte prolifer…
View article: Supplementary Figure 3 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 3 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 3: PPARγ induced expression of ANXA1 and cell death is abrogated in TNBC cells with pre-incubation of a PPARγ-specific antagonist or use of a dominant negative derivative of PPARγ.
View article: Supplementary Figure 5 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 5 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 5: PPARγ ligand-induced expression of ANXA1 interacts with RIP1 blocking RIP1-NEMO interaction leading to deubiquitination of RIP1.
View article: Supplementary Figure 2 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 2 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 2: ANXA1 expressing TNBC cell lines display greater sensitivity to PPARγ ligands compared to ANXA1 depleted cells.
View article: Supplementary Figure 1 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 1 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 1: High ANXA1 and PPARγ expression levels positively correlates with the invasive, high-grade phenotype
View article: Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Metastatic breast cancer is still incurable so far; new specifically targeted and more effective therapies for triple-negative breast cancer (TNBC) are required in the clinic. In this study, our clinical data have established that basal an…
View article: Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Metastatic breast cancer is still incurable so far; new specifically targeted and more effective therapies for triple-negative breast cancer (TNBC) are required in the clinic. In this study, our clinical data have established that basal an…
View article: Supplementary Figure 4 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 4 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 4: PPARγ ligand-induced changes in expression of RIP1 and NEMO and therefore NFκB activity are receptor dependent.
View article: Supplementary Figure 1 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 1 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 1: High ANXA1 and PPARγ expression levels positively correlates with the invasive, high-grade phenotype
View article: Supplementary Figure 3 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 3 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 3: PPARγ induced expression of ANXA1 and cell death is abrogated in TNBC cells with pre-incubation of a PPARγ-specific antagonist or use of a dominant negative derivative of PPARγ.
View article: Supplementary Figure 4 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 4 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 4: PPARγ ligand-induced changes in expression of RIP1 and NEMO and therefore NFκB activity are receptor dependent.
View article: Supplemental Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplemental Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary methods and supplementary figure legends
View article: Supplementary Figure 2 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 2 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 2: ANXA1 expressing TNBC cell lines display greater sensitivity to PPARγ ligands compared to ANXA1 depleted cells.
View article: Supplementary Figure 5 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplementary Figure 5 from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary Figure 5: PPARγ ligand-induced expression of ANXA1 interacts with RIP1 blocking RIP1-NEMO interaction leading to deubiquitination of RIP1.
View article: Supplemental Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers
Supplemental Data from PPARγ Ligand–induced Annexin A1 Expression Determines Chemotherapy Response via Deubiquitination of Death Domain Kinase RIP in Triple-negative Breast Cancers Open
Supplementary methods and supplementary figure legends
View article: Development of 1-(4-(Substituted)piperazin-1-yl)-2-((2-((4-methoxybenzyl)thio)pyrimidin-4-yl)oxy)ethanones That Target Poly (ADP-Ribose) Polymerase in Human Breast Cancer Cells
Development of 1-(4-(Substituted)piperazin-1-yl)-2-((2-((4-methoxybenzyl)thio)pyrimidin-4-yl)oxy)ethanones That Target Poly (ADP-Ribose) Polymerase in Human Breast Cancer Cells Open
A number of uracil amides cleave poly (ADP-ribose) polymerase and therefore novel thiouracil amide compounds were synthesized and screened for the loss of cell viability in a human-estrogen-receptor-positive breast cancer cell line. The sy…
View article: Silencing Acetyl-CoA carboxylase A (ACACA) and Sterol Regulatory Element-binding Protein 1 (SREBP1) Genes Through RNAi Reduce Cholesterol Content in Serum and Eggs of Transgenic Chicken
Silencing Acetyl-CoA carboxylase A (ACACA) and Sterol Regulatory Element-binding Protein 1 (SREBP1) Genes Through RNAi Reduce Cholesterol Content in Serum and Eggs of Transgenic Chicken Open
Cholesterol is synthesized in chicken through de novo lipid biosynthetic pathway where two most important genes viz. SREBP1 and ACACA play immense role. To minimize cholesterol synthesis, RNAi approach was adopted and accordingly, we devel…
View article: Resveratrol for cancer therapy: Challenges and future perspectives
Resveratrol for cancer therapy: Challenges and future perspectives Open
Resveratrol (3,4',5-trihydroxy-trans-stilbene) has been expected to ameliorate cancer and foster breakthroughs in cancer therapy. Despite thousands of preclinical studies on the anticancer activity of resveratrol, little progress has been …
View article: MicroRNA-196a promotes renal cancer cell migration and invasion by targeting BRAM1 to regulate SMAD and MAPK signaling pathways
MicroRNA-196a promotes renal cancer cell migration and invasion by targeting BRAM1 to regulate SMAD and MAPK signaling pathways Open
Rationale: MicroRNAs (miRNAs) are endogenous ~22nt RNAs that play critical regulatory roles in various biological and pathological processes, including various cancers. Their function in renal cancer has not been fully elucidated. It has b…
View article: Novel 1,3,4-oxadiazole Targets STAT3 Signaling to Induce Antitumor Effect in Lung Cancer
Novel 1,3,4-oxadiazole Targets STAT3 Signaling to Induce Antitumor Effect in Lung Cancer Open
Lung cancer is the leading type of malignancy in terms of occurrence and mortality in the global context. STAT3 is an oncogenic transcription factor that is persistently activated in many types of human malignancies, including lung cancer.…
View article: Anti-proliferative activity and characterization data on oxadiazole derivatives
Anti-proliferative activity and characterization data on oxadiazole derivatives Open
This data in brief article explains the anti-cancer activity and characterization of oxadiazoles [1]. The main objective of this article was to provide general synthetic procedures, spectral discussion and physical data on the new oxadiazo…
View article: Sphingosine 1-Phosphate Receptor 2 Induces Otoprotective Responses to Cisplatin Treatment
Sphingosine 1-Phosphate Receptor 2 Induces Otoprotective Responses to Cisplatin Treatment Open
Ototoxicity is a major adverse effect of platinum-based chemotherapeutics and currently, there remains a lack of United States Food and Drug Administration-approved therapies to prevent or treat this problem. In our study, we examined the …
View article: The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges
The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges Open
Epithelial-to-Mesenchymal Transition (EMT) has been shown to be crucial in tumorigenesis where the EMT program enhances metastasis, chemoresistance and tumor stemness. Due to its emerging role as a pivotal driver of tumorigenesis, targetin…
View article: Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways
Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways Open
Fangchinoline (FCN) derived from Stephaniae tetrandrine S. Moore can be employed to treat fever, inflammation, rheumatism arthralgia, edema, dysuria, athlete’s foot, and swollen wet sores. FCN can exhibit a plethora of anti-neoplastic effe…
View article: Functional interplay between YY1 and CARM1 promotes oral carcinogenesis
Functional interplay between YY1 and CARM1 promotes oral carcinogenesis Open
Coactivator associated arginine methyltransferase 1 (CARM1) has been functionally implicated in maintenance of pluripotency, cellular differentiation and tumorigenesis; where it plays regulatory roles by virtue of its ability to coactivate…
View article: Focus on Formononetin: Anticancer Potential and Molecular Targets
Focus on Formononetin: Anticancer Potential and Molecular Targets Open
Formononetin, an isoflavone, is extracted from various medicinal plants and herbs, including the red clover (Trifolium pratense) and Chinese medicinal plant Astragalus membranaceus. Formononetin’s antioxidant and neuroprotective effects un…