scholarly journals T-Box transcription factor Tbx20 regulates a genetic program for cranial motor neuron cell body migration

Development ◽  
2006 ◽  
Vol 133 (24) ◽  
pp. 4945-4955 ◽  
Author(s):  
M.-R. Song ◽  
R. Shirasaki ◽  
C.-L. Cai ◽  
E. C. Ruiz ◽  
S. M. Evans ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Motor Neuron ◽  
Cell Body ◽  
Genetic Program ◽  
T Box ◽  
Neuron Cell Body

Regulation of motor neuron dendrite growth by NMDA receptor activation

Development ◽  
1994 ◽  
Vol 120 (11) ◽  
pp. 3063-3071 ◽  
Author(s):  
R.G. Kalb
Keyword(s):  
Nmda Receptor ◽  
Motor Neuron ◽  
Cell Body ◽  
Motor Neurons ◽  
Receptor Activation ◽  
Dendrite Growth ◽  
Postnatal Life ◽  
Receptor Antagonism ◽  
Neuron Cell Body ◽  
Early Postnatal Life

Spinal motor neurons undergo great changes in morphology, electrophysiology and molecular composition during development. Some of this maturation occurs postnatally when limbs are employed for locomotion, suggesting that neuronal activity may influence motor neuron development. To identify features of motor neurons that might be regulated by activity we first examined the structural development of the rat motor neuron cell body and dendritic tree labeled with cholera toxin-conjugated horseradish peroxidase. The motor neuron cell body and dendrites in the radial and rostrocaudal axes grew progressively over the first month of life. In contrast, the growth of the dendritic arbor/cell and number of dendritic branches was biphasic with overabundant growth followed by regression until the adult pattern was achieved. We next examined the influence of neurotransmission on the development of these motor neuron features. We found that antagonism of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor inhibited cell body growth and dendritic branching in early postnatal life but had no effect on the maximal extent of dendrite growth in the radial and rostrocaudal axes. The effects of NMDA receptor antagonism on motor neurons and their dendrites was temporally restricted; all of our anatomic measures of dendrite structure were resistant to NMDA receptor antagonism in adults. These results suggest that the establishment of mature motor neuron dendritic architecture results in part from dendrite growth in response to afferent input during a sensitive period in early postnatal life.

scholarly journals Assessing the role of the T-box transcription factor Eomes in B cell differentiation during either Th1 or Th2 cell-biased responses

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208343 ◽  
Author(s):  
Lucy Cooper ◽  
Lauren Hailes ◽  
Amania Sheikh ◽  
Colby Zaph ◽  
Gabrielle T. Belz ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
B Cell ◽  
B Cell Differentiation ◽  
T Box ◽  
Th2 Cell

scholarly journals The T Box Transcription Factor TBX2 Promotes Epithelial-Mesenchymal Transition and Invasion of Normal and Malignant Breast Epithelial Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e41355 ◽  
Author(s):  
Bin Wang ◽  
Linsey E. Lindley ◽  
Virneliz Fernandez-Vega ◽  
Megan E. Rieger ◽  
Andrew H. Sims ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Breast Epithelial Cells ◽  
Mesenchymal Transition ◽  
T Box ◽  
Malignant Breast ◽  
Breast Epithelial

scholarly journals High expression level of T-box transcription factor 5 predicts unfavorable survival in stage I and II gastric adenocarcinoma

2015 ◽  
Vol 10 (4) ◽  
pp. 2021-2026 ◽  
Author(s):  
YAN ZHENG ◽  
YUAN-FANG LI ◽  
WEI WANG ◽  
YONG-MING CHEN ◽  
DAN-DAN WANG ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Gastric Adenocarcinoma ◽  
Stage I ◽  
High Expression ◽  
Expression Level ◽  
T Box ◽  
High Expression Level

scholarly journals Multiple malignant tumors in a patient with familial chordoma, a case report

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Nuttavut Sumransub ◽  
Paari Murugan ◽  
Shelly Marette ◽  
Denis R. Clohisy ◽  
Keith M. Skubitz
Keyword(s):  
Transcription Factor ◽  
Cell Carcinoma ◽  
Germ Line ◽  
Malignant Tumors ◽  
Treatment Resistance ◽  
Pulmonary Complications ◽  
Her Family ◽  
T Box ◽  
Epithelial Cancers ◽  
Pleomorphic Sarcoma

Abstract Background Chordoma is a rare bone tumor that is typically resistant to chemotherapy and is associated with genetic abnormalities of the T-box transcription factor T (TBXT) gene, which encodes the transcription factor brachyury. Brachyury is felt to be a major contributor to the development of chordomas. Case presentation We describe a 67-year-old woman who developed an undifferentiated pleomorphic sarcoma in her thigh. Despite treatment with standard chemotherapy regimens, she had a rapidly progressive course of disease with pulmonary metastases and passed away 8 months from diagnosis with pulmonary complications. Her medical history was remarkable in that she had a spheno-occipital chordoma at age 39 and later developed multiple other tumors throughout her life including Hodgkin lymphoma and squamous cell carcinoma and basal cell carcinoma of the skin. She had a family history of chordoma and her family underwent extensive genetic study in the past and were found to have a duplication of the TBXT gene. Conclusions Brachyury has been found to associate with tumor progression, treatment resistance, and metastasis in various epithelial cancers, and it might play roles in tumorigenesis and aggressiveness in this patient with multiple rare tumors and germ line duplication of the TBXT gene. Targeting this molecule may be useful for some malignancies.

scholarly journals Balancing dynamic tradeoffs drives cellular reprogramming

2018 ◽  
Author(s):  
Kimberley N. Babos ◽  
Kate E. Galloway ◽  
Kassandra Kisler ◽  
Madison Zitting ◽  
Yichen Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Motor Neuron ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Cellular Reprogramming ◽  
Cellular Event ◽  
Chemical Factors ◽  
Number Of Cells ◽  
Transcription And Replication

AbstractAlthough cellular reprogramming continues to generate new cell types, reprogramming remains a rare cellular event. The molecular mechanisms that limit reprogramming, particularly to somatic lineages, remain unclear. By examining fibroblast-to-motor neuron conversion, we identify a previously unappreciated dynamic between transcription and replication that determines reprogramming competency. Transcription factor overexpression forces most cells into states that are refractory to reprogramming and are characterized by either hypertranscription with little cell division, or hyperproliferation with low transcription. We identify genetic and chemical factors that dramatically increase the number of cells capable of both hypertranscription and hyperproliferation. Hypertranscribing, hyperproliferating cells reprogram at 100-fold higher, near-deterministic rates. We demonstrate that elevated topoisomerase expression endows cells with privileged reprogramming capacity, suggesting that biophysical constraints limit cellular reprogramming to rare events.

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