Purification of nuclear proteins that bind to cisplatin-damaged DNA. Identity with high mobility group proteins 1 and 2.

Hughes, Edward N.; Engelsberg, Beatrice N.; Billings, Paul C.

doi:10.1016/s0021-9258(18)42242-9

Cited by 155 publications

(42 citation statements)

References 48 publications

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“…HMGB1, which has been considered to be a primary recognition factor of cisplatin-DNA adducts, shows a remarkably high affinity to cisplatin-DNA cross-links. 17 As a multifunctional non-chromatin nuclear protein, HMGB1 acts as a molecular chaperon between distorted DNA and various proteins. 18 In contrast to the stabilisation of chromatin by histones, HMGB1 binds with linker DNA between the chromatin cores and destabilises the compact chromatin DNA.…”

Section: Introductionmentioning

confidence: 99%

HMGB1 bound to cisplatin–DNA adducts undergoes extensive acetylation and phosphorylation in vivo

Ding

Wang

et al. 2015

Chem. Sci.

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Section: Introductionmentioning

confidence: 99%

HMGB1 bound to cisplatin–DNA adducts undergoes extensive acetylation and phosphorylation in vivo

Ding

Wang

et al. 2015

Chem. Sci.

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“…protein, exhibits high affinity for distorted DNA structures like four-way junctions, cisplatin-modified DNA, or hemicatenated DNA loops (Bianchi et al, 1989;Gaillard and Strauss, 2000;Hughes et al, 1992). HMGB1 physically interacts with and stimulates TopoIIa activity on catenated DNA structures (Stros et al, 2007a).…”

Section: Introductionmentioning

confidence: 99%

Genome-Organizing Factors Top2 and Hmo1 Prevent Chromosome Fragility at Sites of S phase Transcription

Bermejo

Capra

González-Huici

et al. 2009

Cell

104

140

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Specialized topoisomerases solve the topological constraints arising when replication forks encounter transcription. We have investigated the contribution of Top2 in S phase transcription. Specifically in S phase, Top2 binds intergenic regions close to transcribed genes. The Top2-bound loci exhibit low nucleosome density and accumulate gammaH2A when Top2 is defective. These intergenic loci associate with the HMG protein Hmo1 throughout the cell cycle and are refractory to the histone variant Htz1. In top2 mutants, Hmo1 is deleterious and accumulates at pericentromeric regions in G2/M. Our data indicate that Top2 is dispensable for transcription and that Hmo1 and Top2 bind in the proximity of genes transcribed in S phase suppressing chromosome fragility at the M-G1 transition. We propose that an Hmo1-dependent epigenetic signature together with Top2 mediate an S phase architectural pathway to preserve genome integrity.

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“…Since HMGB1 is thought to bind to CDDP-binding DNA and repair DNA damage, suppressing HMGB1 was thought to reduce the ability of cancer cells to repair DNA and suppress CDDP resistance [26,27]. However, HMGB1 was found to bind to CDDP-bound DNA, thereby inhibiting the access of the repair molecule complex and suppressing the repair [28,29].…”

Section: Discussionmentioning

confidence: 99%

Role of Metastasis-Related Genes in Cisplatin Chemoresistance in Gastric Cancer

Nishiguchi

Oue

Fujiwara‐Tani

et al. 2019

IJMS

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The role of metastasis-related genes in cisplatin (CDDP) chemoresistance in gastric cancer is poorly understood. Here, we examined the expression of four metastasis-related genes (namely, c-met, HMGB1, RegIV, PCDHB9) in 39 cases of gastric cancer treated with neoadjuvant therapy with CDDP or CDDP+5-fluorouracil and evaluated its association with CDDP responsiveness. Comparison of CDDP-sensitive cases with CDDP-resistant cases, the expression of c-met, HMGB1, and PCDHB9 was correlated with CDDP resistance. Among them, the expression of HMGB1 showed the most significant correlation with CDDP resistance in multivariate analysis. Treatment of TMK-1 and MKN74 human gastric cancer cell lines with ethyl pyruvate (EP) or tanshinone IIA (TAN), which are reported to inhibit HMGB1 signaling, showed a 4–5-fold increase in inhibition by CDDP. Treatment with EP or TAN also suppressed the expression of TLR4 and MyD88 in the HMGB1 signal transduction pathway and suppressed the activity of NFκB in both cell lines. These results suggest that the expression of these cancer metastasis-related genes is also related to anticancer drug resistance and that suppression of HMGB1 may be particularly useful for CDDP sensitization.

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Purification of nuclear proteins that bind to cisplatin-damaged DNA. Identity with high mobility group proteins 1 and 2.

Cited by 155 publications

References 48 publications

HMGB1 bound to cisplatin–DNA adducts undergoes extensive acetylation and phosphorylation in vivo

HMGB1 bound to cisplatin–DNA adducts undergoes extensive acetylation and phosphorylation in vivo

Genome-Organizing Factors Top2 and Hmo1 Prevent Chromosome Fragility at Sites of S phase Transcription

Role of Metastasis-Related Genes in Cisplatin Chemoresistance in Gastric Cancer

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