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Validated All-in-One™ qPCR Primer for ZBTB16(NM_001018011.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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. [provided by RefSeq].
Gene References into function
- two critical hits for promyelocytic leukemia
- PLZF/RARalpha also binds the HD-NCR through the PLZF, which seems to be crucial for the t-RA resistance of t(11;17) APL patients
- can interact with GATA-2 and can modify GATA-2 transactivation capacity
- evidence of a functional interaction between the promyelocytic leukemia zinc finger protein (PLZF) and DRAL/FHL2
- PLZF plays a significant stimulatory role in megakaryocytic development, seemingly mediated in part by induction of TpoR expression at transcriptional level.
- Hoxb2 is a direct target for regulation by PLZF in the developing CNS and suggest that deregulation of Hox gene expression may contribute to APL pathogenesis.
- gene expression regulation in human endometrial stromal cells and myometrial smooth muscle cells
- PLZF colocalizes with SUMO-1 in the nucleus; lysine 242 in the RD2 domain of human PLZF was identified as the sumoylation site
- PLZF expression maintains a cell in a quiescent state by repressing c-myc expression and preventing cell cycle progression.
- An inactive mutant of PLZF abolishes expression of p85 alpha PI3K followed by enhanced p70(S6) kinase.
- a suppressor role in solid tumors
- data indicate that recruitment of HDAC4 is necessary for PLZF-mediated repression in both normal and leukaemic cells
- PLZF plays important roles in early osteoblastic differentiation as an upstream regulator of CBFA1
- Histone acetyltransferase activity of p300 is required for transcriptional repression by PZLF.
- Androgen-independent cell line DU145 cells lack PLZF gene expression, resulting in the upregulation of Pbx1 and HoxC8 expression. The Pbx1-HoxC8 heterocomplex may lead to androgen-independent growth in prostate cancer.
- These data suggest the existence of a mechanism that regulates ERK signaling via the C-terminus of ATP7B and the ATP7B-interacting hepatocytic PLZF.
- potential tumor suppressor activity of CCS-3 may be mediated by its interaction with PLZF.
- existence of a novel signal transduction pathway involving the ligand renin, renin receptor, and the transcription factor PLZF
- The collapsin response mediator protein 1 and the promyelocytic leukemia zinc finger protein interact with UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE).
- TIMP1 regulates cell proliferation by interacting with the ninth zinc finger domain of PZLF.
- Expression of PLZF in corneal endothelial cells is closely related to formation of cell-cell contacts, and PLZF may play role in suppressing their proliferation.
- PLZF upregulates apoptosis-inducer TP53INP1, ID1, and ID3 genes, and downregulates the apoptosis-inhibitor TERT gene
- PLZF mRNA was expressed in HCECs in vivo and in completely confluent HCECs but not in subconfluent HCECs in vitro.
- supports an active role for PLZF and RARalpha-PLZF in leukemogenesis, identifies up-regulation of CRABPI
- Activated Goalpha interacted directly with PLZF, and enhanced its function as a transcriptional and cell growth suppressor.
- PLZF post-translational modification is controlled by intracellular ROS, and the biological function of PLZF is regulated by sumoylation and ubiquitination.
- PLZF negatively regulates the expression of miR-221 and miR-222
- observations suggest that PLZF is a negative regulator of ENaC in renal epithelial cells and might be part of a negative feedback loop that limits aldosterone's stimulatory effects on sodium reabsorption.
- Data indicate that megakaryopoiesis is controlled by a cascade pathway, in which PLZF suppresses miR-146a transcription and thereby activates CXCR4 translation.
- Our findings that PLZF is a key regulator of skeletal and male germline development.
- study suggests that PLZF is a transcriptional signature of NKT cells that directs their innate-like effector differentiation during thymic development
- Increased expression of the tumor suppressor PLZF in malignant melanomas is associated with long-term patient survival.
