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ZNF384 encodes a C2H2-type zinc finger protein, which may function as a transcription factor. Additionally we are shipping Zinc Finger Protein 384 Antibodies (60) and many more products for this protein.
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Ectopic expression of EP300-ZNF384 and CREBBP-ZNF384 fusion altered differentiation of mouse hematopoietic stem and progenitor cells and also potentiated oncogenic transformation in vitro.our results indicate that gene fusion is a common class of genomic abnormalities in childhood ALL and that recurrent translocations involving EP300 and CREBBP may cause epigenetic deregulation with potential for therapeutic targeting.
EP300-ZNF384 mediates GATA3 gene expression and may be involved in the acquisition of the HSC gene expression signature and characteristic immunophenotype in B-cell precursor acute lymphoblastic leukemia cells.
Our observations indicate that ZNF384-related fusion genes consist of a distinct subgroup of B-cell precursor acute lymphoblastic leukemia with a characteristic immunophenotype, while the clinical features depend on the functional properties of individual fusion partners.
the frequency of ZNF384 gene rearrangement in pediatric precursor B cell ALL is approximately 3%.
nuclear matrix protein 4 overexpression increased Aquaporin 5 mRNA expression by 2.5-fold in HEK293 cells
Rare translocation t(12;17)(p13;q12), This translocation has been reported in 25 cases and its putative molecular consequence, the formation of a TAF15-ZNF384 fusion gene, in only six cases.
expression in pelvic lymph nodes and primary tumors in early stage cervical carcinomas
The transcription factor gene CIZ/NMP4 is recurrently involved in acute leukemia through fusion with either EWSR1 or TAF15.
The CIZ protein(also known as ZNF384)was involved and rearrangemented in acute leukemia.
These results suggest that caspase-mediated degradation may represent a novel regulatory mechanism that controls TAF15 and TAF15-CIZ/NMP4 activities.
The heightened osteoanabolism of the Nmp4-/- skeleton enhances the effectiveness of diverse osteoporosis treatments, in part by increasing hyperanabolic osteoprogenitors. Nmp4 provides a promising target pathway for identifying barriers to pharmacologically induced bone formation.
Sustained protein synthesis sensitized cells to pharmacological induction of the Unfolded Protein Response (UPR), and the observed decrease in cell viability was restored upon inhibition of GADD34 activity. We conclude that NMP4 is a key regulator of ribosome biogenesis and the UPR, which together play a central role in determining cell viability during endoplasmic reticulum stress.
NMP4 deficiency suppressed the arthritis-induced increase in bone resorption, expression of RANKL and MMP-3 mRNA.
Nmp4/CIZ limits the parathyroid hormone anabolic window by restricting the number of bone marrow stem, progenitor, and blood cells that support anabolic bone remodeling.
The CIZ/NMP4 expression levels are correlated to the metastatic activity in divergent types of melanoma cells.
Together these results provide experimental support for the concept that Nmp4/CIZ plays an inhibitory role in the response of bone cells to mechanical stimulation induced by OFSS.
Nmp4/CIZ within the context of the PTH-induced anabolic response is described.
localization in the cytoplasm of osteoblasts
Impaired spermatogenesis and male infertility occurred in Nmp4-disrupted mice.
transformation of 3T3 fibroblasts by CIZ/NMP4 fusions is dependent on DNA-binding and might involve transactivation of CIZ target genes
Two adjacent promoters of Nmp4 P(1) [-2521 nucleotide (nt)/-597 nt] and P(2) (-2521 nt/+1 nt) initiate transcription of alternative first exons (U(1) and U(2)).
Histomorphometric analysis revealed that unloading suppressed the levels of osteoblastic bone formation parameters, and such suppression of bone formation parameters was blocked by CIZ-deficiency.
Nmp4 contributes to fluid shear stress induced MMP13 gene induction in osteoblasts.
This gene encodes a C2H2-type zinc finger protein, which may function as a transcription factor. This gene also contains long CAG trinucleotide repeats that encode consecutive glutamine residues. The protein appears to bind and regulate the promoters of the extracellular matrix genes MMP1, MMP3, MMP7 and COL1A1. Studies in mouse suggest that nuclear matrix transcription factors (NP/NMP4) may be part of a general mechanical pathway that couples cell construction and function during extracellular matrix remodeling. Alternative splicing results in multiple transcript variants. Recurrent rearrangements of this gene with the Ewing's sarcoma gene, EWSR1 on chromosome 22, or with the TAF15 gene on chromosome 17, or with the TCF3 (E2A) gene on chromosome 19, have been observed in acute leukemia. A related pseudogene has been identified on chromosome 7.
CAG repeat protein 1
, Cas-interacting zinc finger protein
, expanded repeat domain, CAG/CTG 2
, nuclear matrix transcription factor 4
, trinucleotide repeat-containing gene 1 protein
, nuclear matrix protein 4
, Cas-associated zinc finger protein