HIP1 (Huntingtin Interacting Protein 1)

We found that Hap1 interferes with the phosphorylation of SnRK1 substrates and that two Hap1-interacting effectors, Hip1 and Hip2, enhance its protein stability. We conclude that Hap1 contributes to the reprogramming of maize metabolism and cell cycle, as well as mesophyll cell hypertrophy, by modulating the SnRK1 signaling pathway to regulate starch biosynthesis and host defense responses.

Notably, we demonstrated that NPIDP and topotecan suppress tumor immune evasion both in vitro and in vivo. In summary, our findings reveal the critical role of NCAPH in regulating tumor immune surveillance, suggesting that NCAPH could serve as a potential biomarker and therapeutic target for HNSCC in the future.

Stent placement was effective in improving symptoms, and the best treatment response with alectinib was a partial response. Routine ALK screening using IHC or comprehensive genomic profiling should be considered for patients with lung cancer with suspected ALK gene.

Moreover, MS1-96 effectively enhances the antitumor efficacy of PD-1 antibodies in MC38 CRC models. These findings indicate that MS1-96 offers a potential strategy for advancing tumor immunotherapy.

P1/2, N=30, Not yet recruiting, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School; Nanjing Drum Tower Hospital, The Affiliated Hospital of Nan

Moreover, we found that BATF, combined with the jun proto-oncogene, AP-1 transcription factor subunit (JUN), led to the suppression of huntingtin interacting protein 1-related (HIP1R) expression and the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway. In conclusion, SLC39A5 promotes the progression of GC via the BATF/HIP1R axis, which suggests that SLC39A5 acts as a therapeutic or diagnostic target for GC.

In conclusion, we propose a novel mechanistic insight into the NSUN2/m5C-HIP1 signaling axis that contributes to the pathogenesis of MM. Thus, NSUN2 can be a novel prognostic biomarker in patients with MM and targeting NSUN2 may be a promising therapeutic strategy.

In this study, we used the model organism Caenorhabditis elegans , which is highly amenable to cell biological and genetic approaches, to establish a novel connection between these two regulatory mechanisms and demonstrate the importance of lipid modifications in maintaining the normal functioning of intracellular transport. Our results also provide insights into the fundamental cellular functions of proteins associated with human disease including cancer and metabolic disease.

The presence or absence of comorbid ESRD varies among patients with RAH. However, additional studies are required to validate our results.

Our study also highlighted the involvement of CLTA and EDIL3 in activating the Rap1 signaling pathway, crucial for cancer cell migration, proliferation, and invasion. These findings emphasize the potential of CLTA, EDIL3, HAPLN1, and HIP1 as diagnostic biomarkers and therapeutic targets for TC and HT.

However, there is limited information on the molecular regulators and mechanisms mediated through HIP1 in cancers. In this review, we systematically examine the recent literature on HIP1 to examine its role in various cancer types.

HIP1R is a new gene implicated in RA FLS invasiveness and migration, and regulates unique pathways and cell processes relevant to both RA as well as cancer biology. Our study provides new insight into processes implicated in FLS invasiveness, which is relevant for joint damage in RA, and identify new potential gene targets for FLS-specific treatments.