Results 241 to 250 of about 449,405 (356)

Osteoblast‐CD4+ CTL Crosstalk Mediated by SIRT1/DAAM2 Axis Prevents Age‐Related Bone Loss

open access: yesAdvanced Science, EarlyView.
In the osteoblastic niche, SIRT1 activates and recruits CD4+ CTLs by increasing DAAM2 expression via EZH2 deacetylation and boosting the secretion of key chemokines, such as CCL3, CCL5, and CXCL10. Then, CD4+ CTL directly eliminates senescent osteoblasts in an MHC‐II‐dependent way, thereby slowing down the process of bone ageing and effectively ...
Bin Yang   +20 more
wiley   +1 more source

The crosstalk of caveolin-1 and autophagy in different diseases. [PDF]

open access: yesFront Immunol
Yang Y   +7 more
europepmc   +1 more source

Endogenous MHC Class II Processing of a Viral Nuclear Antigen After Autophagy [PDF]

open access: bronze, 2004
Casper Paludan   +6 more
openalex   +1 more source

Life Factors and Melanoma: From the Macroscopic State to the Molecular Mechanism

open access: yesAdvanced Science, EarlyView.
Melanoma, an aggressive skin cancer, arises from dynamic interactions between genetic, environmental, and lifestyle factors. This review explores how age, gender, obesity, diet, exercise, smoking, alcohol, UV exposure, circadian rhythms, and medications influence melanoma risk and progression.
Hanbin Wang   +4 more
wiley   +1 more source

Ubiquitination‐Dependent LLGL2 Degradation Drives Colorectal Cancer Progression via THBS3 mRNA Stabilization

open access: yesAdvanced Science, EarlyView.
During the progression of CRC, MDM2, as an E3 ubiquitin ligase, promotes the degradation of the LLGL2 protein. Reduced expression of the LLGL2 protein leads to the loss of support for the CNOT1 protein, decreasing the degradation of THBS3 mRNA. The increased THBS3 further activates the PI3K‐Akt pathway, promoting the proliferation and metastasis of CRC.
Jiayan Huang   +8 more
wiley   +1 more source

A Novel Protein Complex Linking the δ2 Glutamate Receptor and Autophagy

open access: bronze, 2002
Zhenyu Yue   +5 more
openalex   +1 more source

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