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tentagel thiol resin (Chem Impex International)

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Chem Impex International tentagel thiol resin
Tentagel Thiol Resin, supplied by Chem Impex International, used in various techniques. Bioz Stars score: 95/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/01741/Polystyrene+resin/us12578345-1406-0-6
Average 95 stars, based on 23 article reviews

tentagel thiol resin - by Bioz Stars, 2026-09

95/100 stars

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Article Title: Single molecule peptide sequencing
Article Snippet: Tentagel Thiol Resin was purchased from Chem-Impex International Incoroporated (USA).

Article Title: Peptoid-Cross-Linked Hydrogel Stiffness Modulates Human Mesenchymal Stromal Cell Immunoregulatory Potential in the Presence of Interferon-Gamma.
Article Snippet: Human mesenchymal stromal cell (hMSC) manufacturing requires the production of large numbers of therapeutically potent cells.. Licensing with soluble cytokines improves hMSC therapeutic potency by enhancing secretion of immunoactive factors but typically decreases proliferative ability.. Soft hydrogels, however, have shown promise for boosting immunomodulatory potential, which may compensate for decreased proliferation.

Article Title: Intra-colony venom diversity contributes to maintaining eusociality in a cooperatively breeding ant
Article Snippet: Rm1a, Rm4a, Rm20a, Rm52d, Rm53a, Rm54a and Rm55a/b were assembled on Rink-amide ProTide resin (CEM, Matthews, NC) to produce a C-terminal amide, whereas Rm9a and Rm34a were assembled on preloaded Wang-polystyrene resin (ChemImpex, Wood Dale, IL), Leu- and Asn, respectively to achieve an acid C-terminal.

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Article Title: Matrix Stiffness Regulates Mechanotransduction and Vascular Network Formation of hiPSC-Derived Endothelial Progenitors Encapsulated in 3D Hydrogels
Article Snippet: .. Following a similar protocol reported by Crosby et al. [ ], RGD (GCGYGRGDSPG) and enzymatically degradable (DGD) peptide (KCGPQGIWGQCK) were synthesized by a Prelude X automated peptide synthesizer (Gyros Protein Technologies) with Rink Amide polystyrene resin (0.48 mmol/g, Chem Impex) as the solid support. ..

Article Title: Tuning Scaffold Degradation with Non-Natural Peptidomimetics to Control Human Umbilical Vein Endothelial Cell Morphology and Vessel Formation
Article Snippet: .. RGD (GCGYGRGDSPG) and peptide/peptoid crosslinkers were all synthesized by a Prelude X automated peptide synthesizer (Gyros Protein Technologies) on Rink Amide polystyrene resin (0.48 mmol g -1 , Chem-Impex) at a scale of 250 μmol. .. Fmoc groups were removed from the Rink Amide resin and subsequent amino acids by washing twice with 20% piperidine (Millipore Sigma) in dimethylformamide (DMF).

Article Title: Tunable hydrogel networks by varying secondary structures of hydrophilic peptoids provide viable 3D cell culture platforms for hMSCs.
Article Snippet: .. A series of peptoids, helical, non-helical, and unstructured (Table 1), were synthesized using Rink Amide polystyrene resin (0.3–0.6 meq g−1, 100–200 mesh from Chem-Impex International, Inc.) on a Prelude X automated peptide synthesizer (Gyros Protein Technologies) at a scale of 250 μM according to previously published submonomer methods.45,46 The syntheses were conducted as follows: fresh bromoacetylation reagent was prepared by dissolving bromoacetic acid (98+%, Thermo Scientific) in dimethylformamide (DMF) (99.8%, Fisher Chemical) at 1.2 M. Bromoacetic acid and N,N′-diisopropylcarbodiimide (DIC) (99.5%, Chem-Impex International, Inc.) were mixed with the resin and heated for 20 minutes before draining and washing with DMF. ..

Article Title: Tunable hydrogel networks by varying secondary structures of hydrophilic peptoids provide viable 3D cell culture platforms for hMSCs
Article Snippet: Overall, this work seeks to establish a biomimetic platform for creating tunable hydrogel systems with decoupled mechanical and structural properties, enabling the systematic study of how matrix mechanics influence hMSC behavior in 3D culture. .. A series of peptoids, helical, non-helical, and unstructured , were synthesized using Rink Amide polystyrene resin (0.3–0.6 meq g −1 , 100–200 mesh from Chem-Impex International, Inc.) on a Prelude X automated peptide synthesizer (Gyros Protein Technologies) at a scale of 250 μM according to previously published submonomer methods. .. The syntheses were conducted as follows: fresh bromoacetylation reagent was prepared by dissolving bromoacetic acid (98+%, Thermo Scientific) in dimethylformamide (DMF) (99.8%, Fisher Chemical) at 1.2 M. Bromoacetic acid and N , N ′-diisopropylcarbodiimide (DIC) (99.5%, Chem-Impex International, Inc.) were mixed with the resin and heated for 20 minutes before draining and washing with DMF.

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Fig. 1 CKMT1 protein was down-regulated in UC and experimental colitis. A Representative images of immunohistochemical staining of colon sections from UC and healthy. B Western blotting analysis of CKMT1 in colonic biopsy tissues from UC (n = 6) and healthy (n = 3), and C in colonic tissues from DSS-induced colitis mice and controls (n = 6). D Representative images of immunoﬂuorescence staining of CKMT1 in colon sections from DSS-induced colitis mice and controls. E Immunoﬂuorescence staining analysis of the co-localization of CKMT1 and Occludin/EpCAM. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Cell death & disease

Article Title: CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis.

doi: 10.1038/s41419-025-07504-4

Figure Lengend Snippet: Fig. 1 CKMT1 protein was down-regulated in UC and experimental colitis. A Representative images of immunohistochemical staining of colon sections from UC and healthy. B Western blotting analysis of CKMT1 in colonic biopsy tissues from UC (n = 6) and healthy (n = 3), and C in colonic tissues from DSS-induced colitis mice and controls (n = 6). D Representative images of immunoﬂuorescence staining of CKMT1 in colon sections from DSS-induced colitis mice and controls. E Immunoﬂuorescence staining analysis of the co-localization of CKMT1 and Occludin/EpCAM. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: The generation of intestinal epithelial-specific Ckmt1 conditional knockout (Ckmt1flox/flox, Vil-Cre) mice (C57BL/6J) was assisted by Cyagen Biosciences (Suzhou, China) through CRISPR/Cas-mediated genome engineering.

Techniques: Immunohistochemical staining, Staining, Western Blot

Fig. 2 Epithelial CKMT1 deﬁciency aggravated DSS-induced colitis in mice. A Targeting strategy for mouse conditional Ckmt1 knockout. (B- C) The knockout was veriﬁed by Western blotting in colon tissues (B) and isolated primary IECs (C) from mice. D Weight curves showing similar growth of male and female CKMT1 KOIEC and WT mice (n = 5 for each group). E Weight loss following DSS treatment was aggravated after epithelial CKMT1 deletion (n = 6–8). F Representative megascopic viewing of colon, and colon length. G DAI scores at day 8. H Evaluation of intestinal barrier function (E-Cadherin, Occludin, and Claudin-1) via Western blotting (n = 6). (I) Immunoﬂuorescent staining of Ly6G and F4/80 in the colon tissues. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Cell death & disease

Article Title: CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis.

doi: 10.1038/s41419-025-07504-4

Figure Lengend Snippet: Fig. 2 Epithelial CKMT1 deﬁciency aggravated DSS-induced colitis in mice. A Targeting strategy for mouse conditional Ckmt1 knockout. (B- C) The knockout was veriﬁed by Western blotting in colon tissues (B) and isolated primary IECs (C) from mice. D Weight curves showing similar growth of male and female CKMT1 KOIEC and WT mice (n = 5 for each group). E Weight loss following DSS treatment was aggravated after epithelial CKMT1 deletion (n = 6–8). F Representative megascopic viewing of colon, and colon length. G DAI scores at day 8. H Evaluation of intestinal barrier function (E-Cadherin, Occludin, and Claudin-1) via Western blotting (n = 6). (I) Immunoﬂuorescent staining of Ly6G and F4/80 in the colon tissues. *P < 0.05; **P < 0.01; ***P < 0.001.

Techniques: Knock-Out, Western Blot, Isolation, Staining

Fig. 3 Epithelial CKMT1 deﬁciency aggravated mitochondrial dysfunction and apoptosis in colitis. A Representative images by transmission electron microscopy showing mitochondrial structural changes in colonic IECs of mice. Quantitative real-time PCR analysis of the expression of key genes involved in B mitochondrial biogenesis (n = 6–10), C mitochondrial dynamics and mitophagy (Pink1) (n = 7–10), and D mitochondrial antioxidant system (n = 7–10). E Western blotting analysis for the protein expressions of mitochondrial antioxidant genes in colon tissues. F Dihydroethidium (DHE) staining showing ROS levels in colon tissues. G Mitochondrial morphology of NCM460 cells with CKMT1 overexpression (CKOE) or control (NC) after TNF-α (50 ng/ml) and CHX (20 μg/mL) treatment for 1 h, was observed via confocal microscopy and analyzed via Image-J software. H TUNEL staining showing the apoptosis levels in colon tissues. *P < 0.05; **P < 0.01; ***P < 0.001. One-way ANOVA with a post hoc LSD test was used for pairwise comparisons.

Journal: Cell death & disease

Article Title: CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis.

doi: 10.1038/s41419-025-07504-4

Figure Lengend Snippet: Fig. 3 Epithelial CKMT1 deﬁciency aggravated mitochondrial dysfunction and apoptosis in colitis. A Representative images by transmission electron microscopy showing mitochondrial structural changes in colonic IECs of mice. Quantitative real-time PCR analysis of the expression of key genes involved in B mitochondrial biogenesis (n = 6–10), C mitochondrial dynamics and mitophagy (Pink1) (n = 7–10), and D mitochondrial antioxidant system (n = 7–10). E Western blotting analysis for the protein expressions of mitochondrial antioxidant genes in colon tissues. F Dihydroethidium (DHE) staining showing ROS levels in colon tissues. G Mitochondrial morphology of NCM460 cells with CKMT1 overexpression (CKOE) or control (NC) after TNF-α (50 ng/ml) and CHX (20 μg/mL) treatment for 1 h, was observed via confocal microscopy and analyzed via Image-J software. H TUNEL staining showing the apoptosis levels in colon tissues. *P < 0.05; **P < 0.01; ***P < 0.001. One-way ANOVA with a post hoc LSD test was used for pairwise comparisons.

Techniques: Transmission Assay, Electron Microscopy, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Staining, Over Expression, Control, Confocal Microscopy, Software, TUNEL Assay

Fig. 5 CKMT1 deﬁciency increased mitochondrial ROS via RET. After treated with TNF-α for 24 h (50 ng/ml), DCFH-DA staining showing cellular ROS levels in (A) Lovo cell, or (B) NCM460 cells, via ﬂow cytometry. After treated with TNF-α for 24 h, MitoSOX staining of mitochondrial ROS (mtROS) was assessed via C ﬂow cytometry in Lovo cells, or D via ﬂuorescence microscopy in NCM460 cells. E The effects of FCCP (100 nM) or diazoxide (200 nM) pretreatment on TNF-α-induced mtROS in siCK Lovo cells were assessed via ﬂow cytometry. F The mtROS levels were measured by ﬂow cytometry in Lovo cells pretreated with rotenone (10 nM). G Illustration of electron transport chain-derived ROS production at complex I via RET. H AOX expression markedly reduced the TNF-α-induced mtROS levels in siCK cell. I NADH/NAD+ ratio was measured in cell lysis via microplate reader (n = 3 or 4), and J MMP (stained with TMRE) was measured via ﬂow cytometry. All ﬂow cytometry experiments were repeated three times. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Cell death & disease

Article Title: CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis.

doi: 10.1038/s41419-025-07504-4

Figure Lengend Snippet: Fig. 5 CKMT1 deﬁciency increased mitochondrial ROS via RET. After treated with TNF-α for 24 h (50 ng/ml), DCFH-DA staining showing cellular ROS levels in (A) Lovo cell, or (B) NCM460 cells, via ﬂow cytometry. After treated with TNF-α for 24 h, MitoSOX staining of mitochondrial ROS (mtROS) was assessed via C ﬂow cytometry in Lovo cells, or D via ﬂuorescence microscopy in NCM460 cells. E The effects of FCCP (100 nM) or diazoxide (200 nM) pretreatment on TNF-α-induced mtROS in siCK Lovo cells were assessed via ﬂow cytometry. F The mtROS levels were measured by ﬂow cytometry in Lovo cells pretreated with rotenone (10 nM). G Illustration of electron transport chain-derived ROS production at complex I via RET. H AOX expression markedly reduced the TNF-α-induced mtROS levels in siCK cell. I NADH/NAD+ ratio was measured in cell lysis via microplate reader (n = 3 or 4), and J MMP (stained with TMRE) was measured via ﬂow cytometry. All ﬂow cytometry experiments were repeated three times. *P < 0.05; **P < 0.01; ***P < 0.001.

Techniques: Staining, Cytometry, Microscopy, Derivative Assay, Expressing, Lysis

$Fig. 6 ROS and mPTP were involved in CKMT1-mediated IECs apoptosis. A Flow cytometry analysis of the opening of mPTP (Calcein ﬂuorescence) in Lovo cells. B Flow cytometry analysis of the effect of NAC pretreatment (5 mM for 3 h) on the opening of mPTP induced by TNF-α in siCK cells. C Flow cytometry analysis of the effect of CsA pretreatment (1 μM for 3 h) on TNF-α-induced mtROS generation in siCK cells. D Assessment of cytochrome c, ATP5A, and SPG7 in cytosolic or mitochondrial fraction of siCK cells after apoptosis induction via Western blotting. E Assessment of AIF and BAX expressions after apoptosis induction via Western blotting. F Assessment of the levels of apoptosis- related proteins in siCK cells upon NAC and CsA pretreatment via western blotting (n = 4). All ﬂow cytometry experiments were repeated three times. *P < 0.05; **P < 0.01; ***P < 0.001.$

Journal: Cell death & disease

Article Title: CKMT1 deficiency contributes to mitochondrial dysfunction and promotes intestinal epithelial cell apoptosis via reverse electron transfer-derived ROS in colitis.

doi: 10.1038/s41419-025-07504-4

Figure Lengend Snippet: Fig. 6 ROS and mPTP were involved in CKMT1-mediated IECs apoptosis. A Flow cytometry analysis of the opening of mPTP (Calcein ﬂuorescence) in Lovo cells. B Flow cytometry analysis of the effect of NAC pretreatment (5 mM for 3 h) on the opening of mPTP induced by TNF-α in siCK cells. C Flow cytometry analysis of the effect of CsA pretreatment (1 μM for 3 h) on TNF-α-induced mtROS generation in siCK cells. D Assessment of cytochrome c, ATP5A, and SPG7 in cytosolic or mitochondrial fraction of siCK cells after apoptosis induction via Western blotting. E Assessment of AIF and BAX expressions after apoptosis induction via Western blotting. F Assessment of the levels of apoptosis- related proteins in siCK cells upon NAC and CsA pretreatment via western blotting (n = 4). All ﬂow cytometry experiments were repeated three times. *P < 0.05; **P < 0.01; ***P < 0.001.

Techniques: Flow Cytometry, Western Blot, Cytometry

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