CALB1 (Calbindin 1)

Together, these results demonstrate that B-HGME offers a powerful tool for spatial systems biology and hypothesis generation in development, immunity, and cancer. The source code of our model is available at https://github.com/zxj8806/B-HGME.

Mechanistically, CALB2 overexpression inhibited NP development by activating the cyclic adenosine monophosphate/cAMP response element-binding protein (cAMP/CREB) signaling pathway. CALB2 overexpression inhibits oxidative stress and promotes microglia transition from M1 to M2 phenotype by activating the cAMP/CREB pathway, which in turn attenuates NP.

Peptide deformylase regulates CYP11B2 expression and aldosterone production. The CALB1-calcium signaling pathway may mediate the effects of peptide deformylase on aldosterone overproduction.

CALB1 regulates prostate cancer progression and radiation response by maintaining calcium homeostasis. Its depletion triggers calcium overload and mitochondrial dysfunction, enhancing radiation sensitivity and identifying CALB1 as a potential therapeutic target.

This study identified variations in biomarker patterns among WT and CKD patients. Understanding biomarker interactions may provide future diagnostic approaches for pediatric kidney conditions.

Our findings suggest that uVTN is a promising and non-invasive biomarker for the diagnosis and monitoring of MBC. While future validation in larger cohorts should be done, these results identify a novel urinary protein that represents the first non-invasive diagnostic test for monitoring BC progression and recurrence.

The CETSA experiment demonstrated the existence of a favorable binding thermal stability between AZD-8055 and MYO1G. This research may identify potential biomarkers for predicting the prognosis of ESCC patients.

To our knowledge, this is the first study to employ an AP-IHC method combined with other standard immunofluorescent staining to co-detect weakly expressed neuronal proteins and other cellular markers in brain tissue and cultured neurons. Additionally, our findings uncover a previously unrecognized neuron-specific pattern of Flt3 expression in the cerebellum, laying the foundation for future mechanistic studies on its role in normal brain development and neurological disorders.

P=N/A, N=60, Active, not recruiting, Professor Zoltan Endre, Nephrology Department at Prince of Wales Hospital

In addition, agathisflavone protected Purkinje neurons from ischemic damage, assessed by calbindin (CB) immunofluorescence. The results demonstrate that agathisflavone protects neuronal and myelin integrity in ischemia, which is associated with the modulation of glial responses in the face of ischemic damage.

In summary, we have successfully identified and comprehensively analyzed a gene signature associated with glutamine metabolism in CRC for the first time. This gene signature consistently and reliably predicts the prognosis of CRC patients, indicating its potential as a metabolic target for individuals with CRC.

There was a time-dependent effect of EMF stimulation on the gene and protein expression. The findings support the beneficial effect of EMF stimulation in the repair process following TBI.