Results 51 to 60 of about 168,312,063 (201)

A context‐dependent modulatory role for eIF6 in acquired resistance to vemurafenib in melanoma

open access: yesFEBS Letters, EarlyView.
Acquired resistance to vemurafenib upregulates the translation factor eIF6 in melanoma cells. Silencing eIF6 in resistant cells reduces proliferation and partially restores drug sensitivity, whereas its overexpression increases sensitivity across melanoma lines regardless of BRAF status, via modulation of mTOR, S6K, and MAPK signaling.
George Kyriakopoulos   +9 more
wiley   +1 more source

Membrane composition and thermodynamic identity as boundaries of life for synthetic cell research

open access: yesFEBS Letters, EarlyView.
What makes a cell a cell? The boundary of a living cell is not just a wall. Read as a Markov blanket, the membrane separates internal from external states, generating identity and non‐equilibrium order. Can this identity be rebuilt from scratch in a synthetic cell?
Caterina Presutti, Bert Poolman
wiley   +1 more source

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Lie Group Symmetries as Integral Transforms of Fundamental Solutions [PDF]

open access: yes
We obtain fundamental solutions for PDEs of the form ut = x uxx +f(x)ux ??xru by showing that if the symmetry group of the PDE is nontrivial, it contains a standard integral transform of the fundamental solution. We show that in this case, the problem of
Mark Craddock, Kelly A Lennox
core  

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

The Method of Fundamental Solutions for Inverse and Moving Rigid Body Problems

open access: yes, 2007
在本論文中,採用基本解法來分析反算及移動剛體之問題。在開始時,將基本解法結合矩陣的條件數來分析反算問題,包含二維拉普拉司方程式、柯西問題、遺失邊界條件和內部資料問題、散佈資料問題以及外型反算識別問題。再者,將基本解法結合穩態的史托克斯例來求解過度指定和不足指定部分邊界的反算史托克斯問題。史托克斯例的係數可以從任意兩個場域變數,例如速度、壓力、渦度或是流線函數來求得。將數值解和解析解加以比較均可以得到良好的結果。 接著,將基本解法與非穩態史托克斯例加以合併,加上對反算問題的數值經驗 ...
陳哲維, Chen, Chi-Wei
core  

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

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