N. Zeleznik-Le

发表

MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25).

M. Osaka, J. Rowley, N. Zeleznik-Le, 1999, Proceedings of the National Academy of Sciences of the United States of America.

Structural mechanism of the bromodomain of the coactivator CBP in p53 transcriptional activation.

Roberto Sanchez, Ze'ev Ronai, Lei Zeng, 2004, Molecular cell.

AF10 is split by MLL and HEAB, a human homolog to a putative Caenorhabditis elegans ATP/GTP-binding protein in an invins(10;11)(p12;q23q12).

N. Zeleznik-Le, S. Bohlander, R. Espinosa, 1996, Blood.

YB-1 DNA-binding protein represses interferon gamma activation of class II major histocompatibility complex genes

N. Zeleznik-Le, J. Ting, A. Brown, 1994, The Journal of experimental medicine.

miR-196b directly targets both HOXA9/MEIS1 oncogenes and FAS tumour suppressor in MLL-rearranged leukaemia

N. Zeleznik-Le, Jiwang Zhang, M. L. Le Beau, 2012, Nature Communications.

MLL repression domain interacts with histone deacetylases, the polycomb group proteins HPC2 and BMI-1, and the corepressor C-terminal-binding protein

N. Zeleznik-Le, Z. Xia, M. Diaz, 2003, Proceedings of the National Academy of Sciences of the United States of America.

Histone H3 lysine 79 methyltransferase Dot1 is required for immortalization by MLL oncogenes.

N. Zeleznik-Le, Wenzheng Zhang, C. Chou, 2010, Cancer research.

Adolescent binge-pattern alcohol exposure alters genome-wide DNA methylation patterns in the hypothalamus of alcohol-naïve male offspring.

N. Zeleznik-Le, Chun-Ki Kim, T. Pak, 2017, Alcohol.

The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression.

N. Zeleznik-Le, Z. Xia, J. Chen, 2005, Proceedings of the National Academy of Sciences of the United States of America.

FAK Is required for c‐Met/β‐catenin‐driven hepatocarcinogenesis

N. Zeleznik-Le, Jiwang Zhang, J. Stauffer, 2015, Hepatology.

BCL6 encodes a sequence‐specific DNA‐binding Protein

N. Zeleznik-Le, C. Bastard, G. Nucifora, 1995, Genes, chromosomes & cancer.

All patients with the T(11;16)(q23;p13.3) that involves MLL and CBP have treatment-related hematologic disorders.

F. Behm, S. Raimondi, J. Rowley, 1997, Blood.

NKG2D signaling certifies effector CD8 T cells for memory formation

N. Zeleznik-Le, Kushal Prajapati, José A. Guevara-Patiño, 2019, Journal of Immunotherapy for Cancer.

An in vivo topoisomerase II cleavage site and a DNase I hypersensitive site colocalize near exon 9 in the MLL breakpoint cluster region.

J. Rowley, N. Zeleznik-Le, R. Strick, 1998, Blood.

Repression of the PDCD2 gene by BCL6 and the implications for the pathogenesis of human B and T cell lymphomas

N. Zeleznik-Le, M. Krasowski, D. Huo, 2007, Proceedings of the National Academy of Sciences.

Expression of CD9 antigen on normal activated human B cells.

N. Zeleznik-Le, R. Metzgar, 1989, Cellular immunology.

Glycogen synthase kinase-3 and leukemia: restoring the balance.

N. Zeleznik-Le, N. Birch, 2010, Cancer cell.

One Step Forward in the Challenging Arena of MLL-AF4 Leukemia.

N. Zeleznik-Le, 2016, Cancer cell.

Identification of complex genomic breakpoint junctions in the t(9;11) MLL-AF9 fusion gene in acute leukemia.

B. Roe, J. Rowley, N. Zeleznik-Le, 1997, Genes, chromosomes & cancer.

Overexpression of Foxn1 attenuates age-associated thymic involution and prevents the expansion of peripheral CD4 memory T cells.

N. Zeleznik-Le, Shubin Zhang, A. Firulli, 2011, Blood.

Overexpression of Foxn 1 attenuates age-associated thymic involution and prevents the expansion of peripheral CD 4 memory T cells

N. Zeleznik-Le, Shubin Zhang, A. Firulli, 2011 .

Breakpoint Cluster Region MLL Site Colocalize Near Exon 9 in the An In Vivo Topoisomerase II Cleavage Site and a DNase I Hypersensitive

J. Rowley, N. Zeleznik-Le, R. Strick, 2010 .

A novel gene, MDS2, is fused to ETV6/TEL in a t(1;12)(p36.1;p13) in a patient with myelodysplastic syndrome

J. Rowley, N. Zeleznik-Le, M. Odero, 2002, Genes, chromosomes & cancer.

Breaking the LSD1/KDM1A addiction: therapeutic targeting of the epigenetic modifier in AML.

N. Zeleznik-Le, A. Lokken, 2012, Cancer cell.

Molecular and Cellular Pathobiology Histone H 3 Lysine 79 Methyltransferase Dot 1 Is Required for Immortalization by MLL Oncogenes

N. Zeleznik-Le, Wenzheng Zhang, C. Chou, 2010 .

BCL6 can repress transcription from the human immunodeficiency virus type I promoter/enhancer region

N. Zeleznik-Le, G. Nucifora, T. McKeithan, 1997, Genes, chromosomes & cancer.

Retroviral transduction model of mixed lineage leukemia fused to CREB binding protein

N. Zeleznik-Le, D. Liedman, Donna Liedman, 2001, Current opinion in hematology.

Importance of a specific amino acid pairing for murine MLL leukemias driven by MLLT1/3 or AFF1/4.

N. Zeleznik-Le, Shubin Zhang, J. Bushweller, 2014, Leukemia research.

N. Zeleznik-Le, Y. Hayashi, G. Nucifora, 1995 .

Cryptic ins(2;11) with clonal evolution showing amplification of 11q23–q25 either on hsr(11) or on dmin, in a patient with AML-M2

N. Zeleznik-Le, M. Ardanaz, M. Odero, 2004, Leukemia.

Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family.

J. Rowley, N. Zeleznik-Le, S. Fears, 1996, Proceedings of the National Academy of Sciences of the United States of America.

Transcriptional regulation of the HLA-DRA gene.

N. Zeleznik-Le, J. Ting, J. Cogswell, 1991, Critical reviews in immunology.

Loss of MLL PHD finger 3 is necessary for MLL-ENL-induced hematopoietic stem cell immortalization.

N. Zeleznik-Le, M. Diaz, J. Chen, 2008, Cancer research.

MicroRNAs in leukemias: emerging diagnostic tools and therapeutic targets.

N. Zeleznik-Le, Yousaf A. Mian, 2010, Current drug targets.

Regulation of mir-196b by MLL and its overexpression by MLL fusions contributes to immortalization.

J. Rowley, N. Zeleznik-Le, Jiwang Zhang, 2009, Blood.

MLL protects CpG clusters from methylation within the Hoxa9 gene, maintaining transcript expression

N. Zeleznik-Le, Z. Xia, M. Diaz, 2008, Proceedings of the National Academy of Sciences.

Transcriptional complexity of the HOXA9 locus.

N. Zeleznik-Le, R. Popovic, F. Erfurth, 2008, Blood cells, molecules & diseases.

Aberrant overexpression and function of the miR-17-92 cluster in MLL-rearranged acute leukemia

Donglin Cao, Miao Sun, Zejuan Li, 2010, Proceedings of the National Academy of Sciences.

Characterization of genomic breakpoints in MLL and CBP in leukemia patients with t(11;16)

J. Rowley, N. Zeleznik-Le, Y. Hayashi, 2004, Genes, chromosomes & cancer.

11q23 translocations split the "AT-hook" cruciform DNA-binding region and the transcriptional repression domain from the activation domain of the mixed-lineage leukemia (MLL) gene.

J. Rowley, N. Zeleznik-Le, A. Harden, 1994, Proceedings of the National Academy of Sciences of the United States of America.

Distribution of 11q23 breakpoints within the MLL breakpoint cluster region in de novo acute leukemia and in treatment-related acute myeloid leukemia: correlation with scaffold attachment regions and topoisomerase II consensus binding sites.

N. Zeleznik-Le, S. Tanabe, J. Rowley, 1996, Blood.

Changchun Du, N. Zeleznik-Le, C. Lavau, 2000, The EMBO journal.

MLL is fused to CBP, a histone acetyltransferase, in therapy-related acute myeloid leukemia with a t(11;16)(q23;p13.3).

D. Housman, J. Rowley, N. Zeleznik-Le, 1997, Proceedings of the National Academy of Sciences of the United States of America.

p27kip1 maintains a subset of leukemia stem cells in the quiescent state in murine MLL‐leukemia

N. Zeleznik-Le, Jiwang Zhang, P. Breslin, 2013, Molecular oncology.

Functional Specificity of CpG DNA-binding CXXC Domains in Mixed Lineage Leukemia*

N. Zeleznik-Le, J. Bushweller, N. Birch, 2013, The Journal of Biological Chemistry.

Structure of the MLL CXXC domain–DNA complex and its functional role in MLL-AF9 leukemia

N. Zeleznik-Le, D. Shultis, T. Cierpicki, 2010, Nature Structural &Molecular Biology.

Bromodomain and histone acetyltransferase domain specificities control mixed lineage leukemia phenotype.

N. Zeleznik-Le, Ming-Ming Zhou, S. Alkan, 2006, Cancer research.

DNA structural properties of AF9 are similar to MLL and could act as recombination hot spots resulting in MLL/AF9 translocations and leukemogenesis.

B. Roe, J. Rowley, N. Zeleznik-Le, 2000, Human molecular genetics.

Characterization of the MLL partner gene AF15q14 involved in t(11;15)(q23;q14)

F. Behm, S. Raimondi, C. Naeve, 2003, Oncogene.

Therapeutic antagonists of microRNAs deplete leukemia-initiating cell activity.

N. Zeleznik-Le, B. Aronow, A. Jegga, 2014, The Journal of clinical investigation.

Analysis of the t(6;11)(q27;q23) in leukemia shows a consistent breakpoint in AF6 in three patients and in the ML‐2 cell line

J. Rowley, N. Zeleznik-Le, R. Espinosa, 1996, Genes, chromosomes & cancer.

The miR-17∼92 cluster contributes to MLL leukemia through the repression of MEIS1 competitor PKNOX1.

N. Zeleznik-Le, Yousaf A. Mian, 2016, Leukemia research.

WEE1 is a validated target of the microRNA miR-17-92 cluster in leukemia.

N. Zeleznik-Le, S. Brockway, 2015, Cancer genetics.

Association between early promoter-specific DNA methylation changes and outcome in older acute myeloid leukemia patients.

N. Zeleznik-Le, J. Radich, Shubin Zhang, 2016, Leukemia research.

MLL: How complex does it get?

N. Zeleznik-Le, R. Popovic, 2005, Journal of cellular biochemistry.

FAK mediates a compensatory survival signal parallel to PI3K-AKT in PTEN-null T-ALL cells.

N. Zeleznik-Le, Jiwang Zhang, P. Breslin, 2015, Cell reports.

Mammalian septins nomenclature.

N. Zeleznik-Le, M. Kennedy, Y. Hayashi, 2002, Molecular biology of the cell.

The human programmed cell death-2 (PDCD2) gene is a target of BCL6 repression: Implications for a role of BCL6 in the down-regulation of apoptosis

Y. Furukawa, N. Zeleznik-Le, A. Montag, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Polymorphisms in the MLL breakpoint cluster region (BCR)

S. Raimondi, M. Relling, J. Rowley, 2003, Human Genetics.

The mixed lineage leukemia (MLL) protein involved in 11q23 translocations contains a domain that binds cruciform DNA and scaffold attachment region (SAR) DNA.

J. Rowley, N. Zeleznik-Le, A. Harden, 1996, Current Topics in Microbiology and Immunology.

Degree of recruitment of DOT1L to MLL-AF9 defines level of H3K79 Di- and tri-methylation on target genes and transformation potential.

N. Zeleznik-Le, Mazhar Adli, Ritambhara Singh, 2015, Cell reports.

A new member of the leucine zipper class of proteins that binds to the HLA DR alpha promoter.

N. Zeleznik-Le, L. Glimcher, J. Ting, 1990, Science.

The partial nontandem duplication of the MLL (ALL1) gene is a novel rearrangement that generates three distinct fusion transcripts in B-cell acute lymphoblastic leukemia.

M. Caligiuri, C. Bloomfield, N. Zeleznik-Le, 2001, Cancer research.

A t(11;15) fuses MLL to two different genes, AF15q14 and a novel gene MPFYVE on chromosome 15

J. Rowley, N. Zeleznik-Le, M. Odero, 2003, Oncogene.

Affinity-purified CCAAT-box-binding protein (YEBP) functionally regulates expression of a human class II major histocompatibility complex gene and the herpes simplex virus thymidine kinase gene.

N. Zeleznik-Le, J. Azizkhan, J. Ting, 1991, Proceedings of the National Academy of Sciences of the United States of America.

Cytogenetic and molecular analysis of the acute monocytic leukemia cell line THP‐1 with an MLL‐AF9 translocation

J. Rowley, N. Zeleznik-Le, M. Odero, 2000, Genes, chromosomes & cancer.

BCOR Binding to MLL-AF9 Is Essential for Leukemia via Altered EYA1, SIX, and MYC Activity.

N. Zeleznik-Le, Shubin Zhang, J. Bushweller, 2020, Blood cancer discovery.

MLL (Mixed Lineage Leukemia Gene) gene

N. Zeleznik-Le, 2002 .

The molecular biology of myeloproliferative disorders as revealed by chromosomal abnormalities.

J. Rowley, N. Zeleznik-Le, G. Nucifora, 1995, Seminars in hematology.

Identification of complex genomic breakpoint junctions in the t(9;11) MLL‐AF9 fusion gene in acute leukemia

B. Roe, J. Rowley, N. Zeleznik-Le, 1997 .

N. Zeleznik-Le, Y. Hayashi, G. Nucifora, 1995, Blood.

FAK Is required for c‐Met/β‐catenin‐driven hepatocarcinogenesis

N. Zeleznik-Le, Jiwang Zhang, J. Stauffer, 2015, Hepatology.

Establishment and characterization of a megakaryoblast cell line with amplification of MLL

N. Zeleznik-Le, T. Veldman, T. Ried, 1998, Leukemia.

Glycogen synthase kinase-3 and leukemia: restoring the balance.

N. Zeleznik-Le, N. Birch, 2010, Cancer cell.