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anti-Human ZBTB16 Antibodies:
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Human Monoclonal ZBTB16 Primary Antibody for FACS - ABIN4895342
Gérart, Sibéril, Martin, Lenoir, Aguilar, Picard, Lantz, Fischer, Latour: Human iNKT and MAIT cells exhibit a PLZF-dependent proapoptotic propensity that is counterbalanced by XIAP. in Blood 2013
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Human Polyclonal ZBTB16 Primary Antibody for DB, ELISA - ABIN548719
Kang, Choi, Kim: Redox-mediated modification of PLZF by SUMO-1 and ubiquitin. in Biochemical and biophysical research communications 2008
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Human Monoclonal ZBTB16 Primary Antibody for ChIP, ICC - ABIN2668927
Koken, Reid, Quignon, Chelbi-Alix, Davies, Kabarowski, Zhu, Dong, Chen, Chen, Tan, Licht, Waxman, de Thé, Zelent: Leukemia-associated retinoic acid receptor alpha fusion partners, PML and PLZF, heterodimerize and colocalize to nuclear bodies. in Proceedings of the National Academy of Sciences of the United States of America 1997
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Human Monoclonal ZBTB16 Primary Antibody for ELISA, PLA - ABIN2773728
Narimatu, Nagata, Sugizaki, Hamasaki: [A new method for immunological detection of fecal blood, using colloidal gold labeled with anti-human hemoglobin monoclonal antibody]. in Rinsho byori. The Japanese journal of clinical pathology 1992
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Human Monoclonal ZBTB16 Primary Antibody for ICC, ELISA - ABIN969465
Felicetti, Errico, Bottero, Segnalini, Stoppacciaro, Biffoni, Felli, Mattia, Petrini, Colombo, Peschle, Carè: The promyelocytic leukemia zinc finger-microRNA-221/-222 pathway controls melanoma progression through multiple oncogenic mechanisms. in Cancer research 2008
Cow (Bovine) Polyclonal ZBTB16 Primary Antibody for WB - ABIN2780737
Deng, Zhang, Kang, Liu, Zhao, Gao, Li, Pan, Tang, Wang, Niu, Yang, Zeng: An unusual haplotype structure on human chromosome 8p23 derived from the inversion polymorphism. in Human mutation 2008
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Human Polyclonal ZBTB16 Primary Antibody for ICC, IF - ABIN4346320
Wasim, Carlet, Mansha, Greil, Ploner, Trockenbacher, Rainer, Kofler: PLZF/ZBTB16, a glucocorticoid response gene in acute lymphoblastic leukemia, interferes with glucocorticoid-induced apoptosis. in The Journal of steroid biochemistry and molecular biology 2010
Human Monoclonal ZBTB16 Primary Antibody for CyTOF, FACS - ABIN4899031
Hsieh, Botta, Gao, Li, Van Allen, Treacy, Cai, He, Sweeney, Brown, Balk, Nelson, Garraway, Kantoff: PLZF, a tumor suppressor genetically lost in metastatic castration-resistant prostate cancer, is a mediator of resistance to androgen deprivation therapy. in Cancer research 2015
Study found that ANRIL expression in gastric cancer cell lines and tumor tissues was negatively associated with the level of PLZF and with ANRILrecruited polycomb repressive complex 2, which then drove PLZF silencing by collaborating between H3K27me3 and DNA methylation.
ZBTB16 is a sensitive and specific marker for yolk sac tumour (YST) and is diagnostically superior to AFP and glypican-3 in metastatic and extragonadal settings.
Selected gene variants of the transcription factor ZBTB16 influence obesity-related parameters and serum lipid levels.
ZBTB16 is a highly sensitive and specific marker for yolk sac tumors.
Low ZBTB16 expression is associated with tongue squamous cell carcinoma.
High PLZF expression is associated with acute myeloid leukemia.
Emerging evidence shows that PLZF regulates the balance of self-renewal and differentiation in stem cells.
integration of PLZF ChIP-Seq and RNA Pol II RNA-Seq datasets revealed that the early growth response 1 (EGR1) transcription factor is a PLZF target for which its level of expression must be reduced to enable progesterone dependent hESC decidualization
NLRP7 is involved in Hydatidiform Molar Pregnancy (HYDM1) and interacts with the transcriptional repressor ZBTB16
These results support a prognostic value for loss of cytoplasmic PLZF expression in the stratification of non-small cell lung cancer and a possible role of cytoplasmic shift and down-regulation of PLZF in the pathogenesis of NSCLC.
down-regulation of PLZF is an important molecular process for prostate tumor progression
Down-regulation of PLZF in human hepatocellular carcinoma.PLZF expression was positively correlated with the alkaline phosphatase level in hepatocellular carcinoma patients.
In dental follicle cells, a Runx2-independent differentiation mechanism exists that is regulated by ZBTB16.
PLZF loss enhances castration-resistant prostate cancer tumor growth in a xenograft model.
Data suggest that interleukin-32alpha (IL-32alpha) associates with leukemia zinc finger (PLZF) and protein kinase c epsilon (PKCvarepsilon), and then inhibits PLZF sumoylation, resulting in suppression of the transcriptional activity of PLZF.
PLZF regulates CCR6 and is critical for the acquisition and maintenance of the Th17 phenotype in human cells.
Authors found that PLZF mediates suppression of miR-146a to control increases of CXCR4 and TRAF6 protein levels in human primary CD4(+) T lymphocytes.
Data indicate that normal ovarian tissues strongly expressed histone H1.5, whereas ovarian granulosa cell tumors (GCTs) weakly expressed this protein; in contrast, PLZF protein expression was not significantly different between both study groups.
When comparing benign and malignant uterine tumors, statistically significant differences were found in staining patterns for PLZF.
a PTEN/PLZF pathway and would shed new lights for developing therapeutic strategy of prostate cancer
Enhanced ZBTB16 promoted both white and brown-like adipogenesis of bovine intramuscular preadipocytes. Increased expressions of adipogenic transcription factors such as PPARgamma, C/EBPalpha, FABP4, and ADIPOQ participated in the pro-adipogenic effects of ZBTB16.
We further find that overexpression of NANOS2 results in the repression of GFRA1 and PLZF in gonocytes, leading to a delay in GST. On the other hand, loss of NANOS2 results in the up-regulation of GFRA1 and PLZF, indicating a precocious entry of GST.
Tnp1, Tekt1, and Plzf have essential roles in spermatogenesis and can be expressed during organ culture of testis; with this system, genes can be induced only at the molecular level and not beyond meiosis.
Zbtb16-encoded transcription factor PLZF directs the differentiation of multiple innate and innate-like cell lineages. Specific Runx1-bound enhancer elements critically modulate lineage-dependent expressions of PLZF.
these findings demonstrate that PLZF controls ROS levels, which in turn governs the inflammatory function of NKT cells
these data reveal the full profile of PLZF and SALL4 regulatory targets in undifferentiated spermatogonia.
Several layers of regulation of the innate-like NKT effector program: First, PLZF bound and regulated genes encoding cytokine receptors as well as homing and adhesion receptors; second, PLZF bound and activated T-helper-specific transcription factor genes that in turn control T-helper-specific programs; finally, PLZF bound and suppressed the transcription of Bach2, a potent general repressor of effector differentiation
Together, these results suggest a novel mechanism regulating endothelial PATZ1 expression based on the down-regulation of miR-24 expression caused by hyperglycemia. Interfering with PATZ1 expression via miRNAs or miRNA mimics could potentially represent a new way to target endothelial PATZ1-dependent signaling of vascular dysfunction in diabetes.
Results clearly indicate that PLZF promotes cell cycle exit and cell differentiation into hypertrophic chondrocytes.
plzf has a role in regulating HSC function that is linked to cell cycle regulation
PLZF expression is highly specific to innate T cells and cannot be induced in conventional T cells via TCR-mediated activation or inflammatory challenge
PLZF expression at the innate lymphoid cell precursor stage has a long-range effect on the functional properties of mature ILC2s and highlights the importance of these cells for innate allergic responses in otherwise immunocompetent mice.
Data suggest that age-related increase in Plzf expression represents a novel molecular signature of spermatogonia aging by functionally arresting their differentiation.
Data indicate the function of promyelocytic leukaemia zinc finger PLZF in the development of innate-like interleukin-17, TcR gamma-delta (IL-17+Vgamma6+ gammadelta) T cells.
The data suggest that Pak2 controls thymic Natural Killer T-cell development by providing a signal that links Egr2 to induce PLZF, in part by regulating signaling lymphocyte activation molecule 6 expression.
The acetyltransferase HAT1 moderates the NF-kappaB inflammatory response by regulating the transcription factor PLZF.
G-protein-coupled receptors, such as CXCR4, regulate autophagy by ZBTB16-mediated ubiquitination and proteasomal degradation of Atg14L .
Data conclude that PLZF is a critical regulator of hepatic gluconeogenesis.
Jarid2 is a novel player in iNKT cell maturation that regulates PLZF expression by modulating H3K9 methylation
Dynamic upregulation of let-7 miRNAs during the development of NKT thymocytes downregulated PLZF expression and directed their terminal differentiation into interferon-gamma (IFN-gamma)-producing NKT1 cells.
PLZF together with other, yet to be defined, factors contribute to the divergence between innate lymphoid cells (ILC) type 1 lineages.
the results provide strong evidence that zbtb16a loss of function is associated with a partially penetrant severe cardiac development defect.
Although zbtb16a and zbtb16b are not modulated by IFN produced during viral infection, their over-expression increases the level of the early type I IFN response, at a critical phase in the race between the virus and the host response.
This gene is a member of the Krueppel C2H2-type zinc-finger protein family and encodes a zinc finger transcription factor that contains nine Kruppel-type zinc finger domains at the carboxyl terminus. This protein is located in the nucleus, is involved in cell cycle progression, and interacts with a histone deacetylase. Specific instances of aberrant gene rearrangement at this locus have been associated with acute promyelocytic leukemia (APL). Alternate transcriptional splice variants have been characterized.
zinc finger and BTB domain-containing protein 16
, zinc finger protein 145 (Kruppel-like, expressed in promyelocytic leukemia)
, zinc finger protein PLZF
, promyelocytic leukemia zinc finger protein
, Green's luxoid
, zinc finger protein 145
, Polydactyly-luxate syndrome
, promyelocytic leukemia zinc finger
, zinc finger and BTB domain containing 16 protein
, promyelocytic leukemia zinc finger protein-A
, zinc finger and BTB domain containing 16
, zinc finger and BTB domain-containing protein 16-A
, zinc finger protein PLZF-A