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Peptide-Based Regulation of TNF-α-Mediated Cytotoxicity
by
Temur, Betul Zehra
, Timucin, Ahmet Can
, Can, Ozge
, Kocagoz, Tanil
, Atik, Ahmet Emin
in
Adalimumab
/ Amino acids
/ Animals
/ Apoptosis
/ Apoptosis - drug effects
/ Cell growth
/ Cell Line
/ Comparative analysis
/ Cytotoxicity
/ Enzymes
/ Humans
/ Inflammatory diseases
/ Kinases
/ Mice
/ Peptides
/ Peptides - chemistry
/ Peptides - pharmacology
/ Protein Binding
/ Proteins
/ Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type I - metabolism
/ Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type II - chemistry
/ Receptors, Tumor Necrosis Factor, Type II - metabolism
/ Rheumatoid arthritis
/ Simulation
/ Synthetic peptides
/ TNF-α
/ TNF-α inhibition
/ TNF-α receptors
/ TNF-α-binding peptide
/ TNFR1-binding peptide
/ TNFR2-binding peptide
/ Tumor necrosis factor
/ Tumor necrosis factor receptors
/ Tumor Necrosis Factor-alpha - metabolism
/ Tumor Necrosis Factor-alpha - pharmacology
/ Tumor necrosis factor-α
2025
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Peptide-Based Regulation of TNF-α-Mediated Cytotoxicity
by
Temur, Betul Zehra
, Timucin, Ahmet Can
, Can, Ozge
, Kocagoz, Tanil
, Atik, Ahmet Emin
in
Adalimumab
/ Amino acids
/ Animals
/ Apoptosis
/ Apoptosis - drug effects
/ Cell growth
/ Cell Line
/ Comparative analysis
/ Cytotoxicity
/ Enzymes
/ Humans
/ Inflammatory diseases
/ Kinases
/ Mice
/ Peptides
/ Peptides - chemistry
/ Peptides - pharmacology
/ Protein Binding
/ Proteins
/ Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type I - metabolism
/ Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type II - chemistry
/ Receptors, Tumor Necrosis Factor, Type II - metabolism
/ Rheumatoid arthritis
/ Simulation
/ Synthetic peptides
/ TNF-α
/ TNF-α inhibition
/ TNF-α receptors
/ TNF-α-binding peptide
/ TNFR1-binding peptide
/ TNFR2-binding peptide
/ Tumor necrosis factor
/ Tumor necrosis factor receptors
/ Tumor Necrosis Factor-alpha - metabolism
/ Tumor Necrosis Factor-alpha - pharmacology
/ Tumor necrosis factor-α
2025
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Peptide-Based Regulation of TNF-α-Mediated Cytotoxicity
by
Temur, Betul Zehra
, Timucin, Ahmet Can
, Can, Ozge
, Kocagoz, Tanil
, Atik, Ahmet Emin
in
Adalimumab
/ Amino acids
/ Animals
/ Apoptosis
/ Apoptosis - drug effects
/ Cell growth
/ Cell Line
/ Comparative analysis
/ Cytotoxicity
/ Enzymes
/ Humans
/ Inflammatory diseases
/ Kinases
/ Mice
/ Peptides
/ Peptides - chemistry
/ Peptides - pharmacology
/ Protein Binding
/ Proteins
/ Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type I - metabolism
/ Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type II - chemistry
/ Receptors, Tumor Necrosis Factor, Type II - metabolism
/ Rheumatoid arthritis
/ Simulation
/ Synthetic peptides
/ TNF-α
/ TNF-α inhibition
/ TNF-α receptors
/ TNF-α-binding peptide
/ TNFR1-binding peptide
/ TNFR2-binding peptide
/ Tumor necrosis factor
/ Tumor necrosis factor receptors
/ Tumor Necrosis Factor-alpha - metabolism
/ Tumor Necrosis Factor-alpha - pharmacology
/ Tumor necrosis factor-α
2025
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Journal Article
Peptide-Based Regulation of TNF-α-Mediated Cytotoxicity
2025
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Overview
Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine associated with TNF receptor 1 (TNFR1) and TNF receptor 2 (TNFR2), which play important roles in several inflammatory diseases. There is a growing interest in developing alternative molecules that can be used as TNF blockers. In this study, we focused on TNF-α-, TNFR1-, and TNFR2-mimicking peptides to inhibit TNF-α receptor binding in various ways. Six peptides (OB1, OB2, OB5, OB6, OB7, and OB8) were developed to bind TNFR1, TNFR2, and TNF-α. OB1 and OB2 bound to TNF-α with lower Kd values of 300 and 46.7 nM, respectively, compared to previously published sequences. These synthetic peptides directly and indirectly inhibited TNF-α in vitro without cytotoxicity to L929 cells, and OB1 significantly inhibited apoptosis in the presence of hTNF-α. Peptides developed in this study may prove to be useful for therapeutic inhibition of TNF-α.
Publisher
MDPI AG,MDPI
Subject
/ Animals
/ Enzymes
/ Humans
/ Kinases
/ Mice
/ Peptides
/ Proteins
/ Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type I - metabolism
/ Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors
/ Receptors, Tumor Necrosis Factor, Type II - chemistry
/ Receptors, Tumor Necrosis Factor, Type II - metabolism
/ TNF-α
/ Tumor necrosis factor receptors
/ Tumor Necrosis Factor-alpha - metabolism
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