scholarly journals A Homeodomain-Zinc Finger Protein, ZFHX4, Is Expressed in Neuronal Differentiation Manner and Suppressed in Muscle Differentiation Manner

2006 ◽  
Vol 29 (9) ◽  
pp. 1830-1835 ◽  
Author(s):  
Kazunori Hemmi ◽  
Dongping Ma ◽  
Yutaka Miura ◽  
Makoto Kawaguchi ◽  
Masakiyo Sasahara ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Muscle Differentiation ◽  
Finger Protein

scholarly journals Zfp422 promotes skeletal muscle differentiation by regulating EphA7 to induce appropriate myoblast apoptosis

2019 ◽  
Vol 27 (5) ◽  
pp. 1644-1659 ◽  
Author(s):  
Yaping Nie ◽  
Shufang Cai ◽  
Renqiang Yuan ◽  
Suying Ding ◽  
Xumeng Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Zinc Finger ◽  
Muscle Development ◽  
Zinc Finger Protein ◽  
Critical Role ◽  
Muscle Differentiation ◽  
C2c12 Cells ◽  
Myoblast Differentiation ◽  
Skeletal Muscle Differentiation ◽  
Finger Protein

Abstract Zinc finger protein 422 (Zfp422) is a widely expressed zinc finger protein that serves as a transcriptional factor to regulate downstream gene expression, but until now, little is known about its roles in myogenesis. We found here that Zfp422 plays a critical role in skeletal muscle development and regeneration. It highly expresses in mouse skeletal muscle during embryonic development. Specific knockout of Zfp422 in skeletal muscle impaired embryonic muscle formation. Satellite cell-specific Zfp422 deletion severely inhibited muscle regeneration. Myoblast differentiation and myotube formation were suppressed in Zfp422-deleted C2C12 cells, isolated primary myoblasts, and satellite cells. Chromatin Immunoprecipitation Sequencing (ChIP-Seq) revealed that Zfp422 regulated ephrin type-A receptor 7 (EphA7) expression by binding an upstream 169-bp DNA sequence, which was proved to be an enhancer of EphA7. Knocking EphA7 down in C2C12 cells or deleting Zfp422 in myoblasts will inhibit cell apoptosis which is required for myoblast differentiation. These results indicate that Zfp422 is essential for skeletal muscle differentiation and fusion, through regulating EphA7 expression to maintain proper apoptosis.

scholarly journals X-MyT1, a Xenopus C2HC-Type Zinc Finger Protein with a Regulatory Function in Neuronal Differentiation

Cell ◽  
1996 ◽  
Vol 87 (7) ◽  
pp. 1191-1202 ◽  
Author(s):  
Eric J Bellefroid ◽  
Catherine Bourguignon ◽  
Thomas Hollemann ◽  
Qiufu Ma ◽  
David J Anderson ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Regulatory Function ◽  
Finger Protein

Identification of NKL, a novel Gli-Kruppel zinc-finger protein that promotes neuronal differentiation

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1335-1346 ◽  
Author(s):  
E. Lamar ◽  
C. Kintner ◽  
M. Goulding
Keyword(s):  
Neuronal Differentiation ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Primary Neurons ◽  
In Ovo ◽  
Neuronal Markers ◽  
Helix Loop Helix ◽  
Finger Protein ◽  
Neuronal Precursors ◽  
Vp16 Fusion

The proneural basic helix-loop-helix proteins play a crucial role in promoting the differentiation of postmitotic neurons from neural precursors. However, recent evidence from flies and frogs indicates that additional factors act together with the proneural bHLH proteins to promote neurogenesis. We have identified a novel zinc finger protein, neuronal Kruppel-like protein (NKL), that positively regulates neurogenesis in vertebrates. NKL is expressed in Xenopus primary neurons and in differentiating neuronal precursors in the intermediate zone of the mouse and chick neural tube. In frog embryos, NKL is induced by overexpression of Neurogenin (Ngn), arguing that NKL is downstream of the proneural determination genes. Our results show that NKL and a NKL/VP16 fusion protein promote differentiation of neuronal precursors in the embryonic chick spinal cord. Following in ovo misexpression of NKL, neuroepithelial cells exit the cell cycle and differentiate into neurons. Similarly, NKL/VP16 induces extra primary neurons in frogs and upregulates expression of the neural differentiation factors, Xath3 and MyT1, as well as the neuronal markers, N-tubulin and elrC. Our findings establish NKL as a novel positive regulator of neuronal differentiation and provide further evidence that non-bHLH transcription factors function in the neuronal differentiation pathway activated by the vertebrate neuronal determination genes.

scholarly journals ZNF536, a Novel Zinc Finger Protein Specifically Expressed in the Brain, Negatively Regulates Neuron Differentiation by Repressing Retinoic Acid-Induced Gene Transcription

2009 ◽  
Vol 29 (13) ◽  
pp. 3633-3643 ◽  
Author(s):  
Zhen Qin ◽  
Fangli Ren ◽  
Xialian Xu ◽  
Yongming Ren ◽  
Hongge Li ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Marker Genes ◽  
Specific Gene ◽  
Specific Marker ◽  
Neuron Differentiation ◽  
Finger Protein ◽  
The Brain

ABSTRACT Neuronal differentiation is tightly regulated by a variety of factors. In a search for neuron-specific genes, we identified a highly conserved novel zinc finger protein, ZNF536. We observed that ZNF536 is most abundant in the brain and, in particular, is expressed in the developing central nervous system and dorsal root ganglia and localized in the cerebral cortex, hippocampus, and hypothalamic area. During neuronal differentiation of P19 cells induced by retinoic acid (RA), ZNF536 expression is increased at an early stage, and it is maintained at a constant level in later stages. Overexpression of ZNF536 results in an inhibition of RA-induced neuronal differentiation, while depletion or mutation of the ZNF536 gene results in an enhancement of differentiation. We further demonstrated that ZNF536 inhibits expression of neuron-specific marker genes, possibly through the inhibition of RA response element-mediated transcriptional activity, as overexpression of RA receptor α can rescue the inhibitory role of ZNF536 in neuronal differentiation and neuron-specific gene expression. Our studies have identified a novel zinc finger protein that negatively regulates neuron differentiation.

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