Results 61 to 70 of about 34,891 (226)

Super‐Enhancer‐Driven SOX4/SMAD3 Mediate Membrane Remodeling by Regulating Phospholipid Metabolism to Accelerate Leukemia Progression

open access: yesAdvanced Science, EarlyView.
Chronic myeloid leukemia blast phase (CML‐BP) poses a severe therapeutic challenge. This study reveals that the super‐enhancer‐driven transcription factors SOX4 and SMAD3 form a cooperative axis critical for disease progression. They co‐activate the oncogenic kinase AXL and promote phospholipid remodeling via LPCAT1 to facilitate its signaling ...
Enzhe Lou   +22 more
wiley   +1 more source

Loss of SOCS1 in Donor T Cells Exacerbates Intestinal GVHD by Driving a Chemokine‐Dependent Pro‐Inflammatory Immune Microenvironment

open access: yesAdvanced Science, EarlyView.
T cell‐specific Socs1 knockout leads to inflammatory differentiation of CD8+ T cells, prompting the STAT1/2 complex to drive the activation of Ccl5, Ccr5, and Cxcr3, and promoting the skewing of monocytes toward a pro‐inflammatory M1 macrophage lineage.
Zhigui Wu   +14 more
wiley   +1 more source

Single‐Cell Profiling Across Immune Tissues and Organs Reveals Immunosenescence Signatures in Male Rhesus Monkeys

open access: yesAdvanced Science, EarlyView.
Single‐cell profiling across bone marrow, spleen, mesenteric lymph, and blood in rhesus monkeys reveals organ Immunosenescence. GZMB rises with age, particularly in cytotoxic and terminally exhausted CD8+ T cells, and BHLHE40 emerges as a key transcription factor enriched across multiple CD8+ subsets, regulating pro‐inflammatory and exhaustion‐related ...
Shengnan Wang   +10 more
wiley   +1 more source

BCR-ABL affects STAT5A and STAT5B differentially. [PDF]

open access: yesPLoS ONE, 2014
Signal transducers and activators of transcription (STATs) are latent cytoplasmic transcription factors linking extracellular signals to target gene transcription. Hematopoietic cells express two highly conserved STAT5-isoforms (STAT5A/STAT5B), and STAT5
Michael Schaller-Schönitz   +9 more
doaj   +1 more source

Targeting Lactate and Lactylation in Cancer Metabolism and Immunotherapy

open access: yesAdvanced Science, EarlyView.
Lactate, once deemed a metabolic waste, emerges as a central regulator of cancer progression. This review elucidates how lactate and its epigenetic derivative, protein lactylation, orchestrate tumor metabolism, immune suppression, and therapeutic resistance.
Jiajing Gong   +5 more
wiley   +1 more source

Dual-Specificity Phosphatase 4 Regulates STAT5 Protein Stability and Helper T Cell Polarization.

open access: yesPLoS ONE, 2015
Immune responses are critically regulated by the functions of CD4 helper T cells. Based on their secreted cytokines, helper T cells are further categorized into different subsets like Treg or Th17 cells, which suppress or promote inflammatory responses ...
Wan-Yi Hsiao   +4 more
doaj   +1 more source

Acetylation and sumoylation control STAT5 activation antagonistically [PDF]

open access: yesJAK-STAT, 2012
STAT5 proteins are activated by tyrosine phosphorylation, but recently further post-translation modifications such as serine/threonine phosphorylation, acetylation at lysine residues or sumoylation in close vicinity of the critical tyrosine residue have been reported.
Krämer, Oliver H., Moriggl, Richard
openaire   +2 more sources

BCR::ABL1‐Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B‐ALL Cells to Enhancer‐Targeting Drugs

open access: yesAdvanced Science, EarlyView.
Ng et al. show that the BCR::ABL1 kinase that drives the lymphoid leukemia Ph+B‐ALL modulates enhancer function by coopting signaling‐inducible transcription factors such as MYC, STAT5, and ETV5. BCR::ABL1 thereby promotes the transcriptional program driving and defining this leukemia and renders Ph+B‐ALL cells hypersensitive to enhancer‐inhibiting ...
Han Leng Ng   +19 more
wiley   +1 more source

STAT5 fits the RISK profile for cardioprotection [PDF]

open access: yesJAK-STAT, 2012
How wonderful would it be if there were a simple, cheap, safe, non-invasive treatment that could be administered to a patient to protect their organs from ischemia and reperfusion? Such a treatment might be used to protect the organs during temporary loss of blood flow, as occurs for example during a heart attack or stroke.
Davidson, Sean M., Yellon, Derek M.
openaire   +2 more sources

T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities

open access: yesAdvanced Science, EarlyView.
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu   +7 more
wiley   +1 more source

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