Zi-Qiang Zhou

The role of senescence and prosurvival signaling in controlling the oncogenic activity of FGFR2 mutants associated with cancer and birth defects (2009)

Ota, Sara, Zhou, Zi-Qiang, Link, Jason M., Hurlin, Peter J.

Mutations in fibroblast growth factor receptors (FGFRs) cause human birth defect syndromes and are associated with a variety of cancers. Although forced expression of mutant activated FGFRs has been...

Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome (2004)

Toyo-oka, Kazuhito, Hirotsune, Shinji, Gambello, Michael J., Zhou, Zi-Qiang, Olson, Lorin, Rosenfeld, Michael G., ...

The Mnt gene encodes a Mad-family bHLH transcription factor located on human 17p13.3. Mnt is one of twenty genes deleted in a heterozygous fashion in Miller-Dieker syndrome (MDS), a contiguous gene...

Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome (2004)

Toyo-oka, Kazuhito, Hirotsune, Shinji, Gambello, Michael J., Zhou, Zi-Qiang, Olson, Lorin, Rosenfeld, Michael G., ...

The Mnt gene encodes a Mad-family bHLH transcription factor located on human 17p13.3. Mnt is one of 20 genes deleted in a heterozygous fashion in Miller–Dieker syndrome (MDS), a contiguous gene...

Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome (2004)

Toyo-oka, Kazuhito, Hirotsune, Shinji, Gambello, Michael J., Zhou, Zi-Qiang, Olson, Lorin, Rosenfeld, Michael G., ...

The Mnt gene encodes a Mad-family bHLH transcription factor located on human 17p13.3. Mnt is one of twenty genes deleted in a heterozygous fashion in Miller-Dieker syndrome (MDS), a contiguous gene...

DNA repair gene expression in baboon tissues and characterization of the baboon XRCC1 promoter :--a dissertation /--Zi-Qiang Zhou. (1997)

Zhou, Zi-Qiang.

Vita.

Spontaneous hepatocellular carcinoma is reduced in transgenic mice overexpressing human O6- methylguanine-DNA methyltransferase

Zhou, Zi-Qiang, Manguino, Diwi, Kewitt, Kristen, Intano, Gabriel W., McMahan, C. Alex, Herbert, Damon C., ...

O6-methylguanine (O6mG) is a potent mutagenic and procarcinogenic DNA lesion. Organisms have evolved with a DNA repair mechanism that largely ameliorates the deleterious effects of O6mG through a...

Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis

Hurlin, Peter J., Zhou, Zi-Qiang, Toyo-oka, Kazuhito, Ota, Sara, Walker, William L., Hirotsune, Shinji, ...

Mnt is a Max-interacting transcriptional repressor that has been hypothesized to function as a Myc antagonist. To investigate Mnt function we deleted the Mnt gene in mice. Since mice lacking Mnt were...

Spontaneous hepatocellular carcinoma is reduced in transgenic mice overexpressing human O6- methylguanine-DNA methyltransferase

Zhou, Zi-Qiang, Manguino, Diwi, Kewitt, Kristen, Intano, Gabriel W., McMahan, C. Alex, Herbert, Damon C., ...

O6-methylguanine (O6mG) is a potent mutagenic and procarcinogenic DNA lesion. Organisms have evolved with a DNA repair mechanism that largely ameliorates the deleterious effects of O6mG through a...

Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis

Hurlin, Peter J., Zhou, Zi-Qiang, Toyo-oka, Kazuhito, Ota, Sara, Walker, William L., Hirotsune, Shinji, ...

Mnt is a Max-interacting transcriptional repressor that has been hypothesized to function as a Myc antagonist. To investigate Mnt function we deleted the Mnt gene in mice. Since mice lacking Mnt were...

Mnt–Max to Myc–Max complex switching regulates cell cycle entry

Walker, William, Zhou, Zi-Qiang, Ota, Sara, Wynshaw-Boris, Anthony, Hurlin, Peter J.

The c-Myc oncoprotein is strongly induced during the G0 to S-phase transition and is an important regulator of cell cycle entry. In contrast to c-Myc, the putative Myc antagonist Mnt is maintained at...

The role of senescence and prosurvival signaling in controlling the oncogenic activity of FGFR2 mutants associated with cancer and birth defects

Ota, Sara, Zhou, Zi-Qiang, Link, Jason M., Hurlin, Peter J.

Mutations in fibroblast growth factor receptors (FGFRs) cause human birth defect syndromes and are associated with a variety of cancers. Although forced expression of mutant activated FGFRs has been...