Aberrant expression of the TLX1/HOX11 proto-oncogene is associated with a significant subset of T-cell acute lymphoblastic leukemias (T-ALL). Yet the manner in which TLX1 contributes to oncogenesis is not fully understood. Since, typically, interactions of HOX and TALE homeodomain proteins are determinant of HOX function, and HOX/MEIS co-expression has been shown to accelerate some leukemias, we systematically examined whether TLX1 interacts with MEIS and PBX proteins. Here, we report that TLX1 and MEIS proteins both interact and are co-expressed in T-ALL, and suggest that co-operation between TLX1 and MEIS proteins may have a significant role in T-cell leukemogenesis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.leukres.2009.06.003 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio De Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) is the leading cause of dementia in elderly humans worldwide. More than 40 million people currently suffer from AD, and this prevalence tends to increase considerably in the coming decades due to increased longevity. The unfolded protein response (UPR) is an adaptive signaling mechanism that aims to maintain cell viability under misfolded protein accumulation and endoplasmic reticulum stress.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Background: The proteasome plays key roles in synaptic plasticity and memory by regulating protein turnover, quality control, and elimination of oxidized/misfolded proteins. Here, we investigate proteasome function and localization at synapses in Alzheimer's disease (AD) post-mortem brain tissue and in experimental models.
Method: We used primary hippocampal cultures, amyloid-β oligomers (AβO)-injected or transgenic animal models, and human brain tissue to determine brain proteasome function and subcellular localization.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio De Janeiro, Rio de Janeiro, Brazil.
Background: Age-related decrease glucose utilization, coupled with insulin resistance, are key features of AD, resulting in reduced glucose utilization/catabolism and oxidative stress generation. Irisin, an exercise-induced hormone promoting mitochondrial biogenesis in adipocytes via PGC-1α, stimulates thermogenic pathways, increases energy expenditure and induces browning of adipose tissue. Further, irisin expression was shown to trigger neuroprotection in AD models.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Rio de Janeiro, Brazil.
Background: The apolipoprotein ε4 (ApoE4) allele is a major risk factor for sporadic Alzheimer's disease (AD) and was shown to promote amyloid-β (Aβ) accumulation and mediate pathophysiological processes in AD. Although the molecular interaction between Aβ and ApoE is acknowledged, the precise nature of this interaction remains unclear. This study aims to explore the biophysical and biochemical nature of the interaction between Aβ and ApoE in the ε3 and ε4 isoforms.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio De Janeiro, Rio de Janeiro, Brazil.
Background: Physical exercise has been proposed as an approach to reduce the risk of Alzheimer's disease (AD). Engaging in physical exercise triggers the shedding of the extracellular domain of fibronectin type III domain-containing protein 5 (FNDC5), producing a circulating peptide (irisin) that promotes neuroprotection in AD mouse models. Despite recent evidence indicating that reduced FNDC5/irisin levels in brain and cerebrospinal fluid correlate with amyloid beta pathology, the impact of FNDC5/irisin on tau pathology remains uncertain.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!