RUFY4

Last update 08 May 2025

Basic Info

Synonyms

FLJ46536, RUFY4, RUN and FYVE domain containing 4

+ [2]

Introduction

Positively regulates macroautophagy in primary dendritic cells. Increases autophagic flux, probably by stimulating both autophagosome formation and facilitating tethering with lysosomes. Binds to phosphatidylinositol 3-phosphate (PtdIns3P) through its FYVE-type zinc finger.

100 Clinical Results associated with RUFY4

100 Translational Medicine associated with RUFY4

0 Patents (Medical) associated with RUFY4

Literatures (Medical) associated with RUFY4

01 Jun 2024·Journal of Cellular Physiology

Identification of binding partners that facilitate membrane‐type 5 matrix metalloproteinase (MT5‐MMP) processing of amyloid precursor protein

Article

Author: Lakshmana, Madepalli K ; Fields, Gregg B ; Wang, Hongjie

AbstractOne of the pathological hallmarks of Alzheimer's disease (AD) is the presence of extracellular deposits of amyloid beta (Aβ) peptide. In addition to Aβ as the core component of the amyloid plaque, the amyloid precursor protein (APP) processing fragment Aβ was also found accumulated around the plaque. The APPη pathway, mainly mediated by membrane‐type 5 matrix metalloproteinase (MT5‐MMP), represents an important factor in AD pathogenesis. The proamyloidogenic features of MT5‐MMP could result from interactions with APP when trafficking between organelles, so determination of the location within the cell of APPη cleavage and interacting proteins of MT5‐MMP affecting this process will be of priority in understanding the role of MT5‐MMP in AD. In the present study, MT5‐MMP was found to be located in the nucleus, cytosol, and cytosolic subcellular granules of CHO cells that stably expressed wild‐type human APP751. MT5‐MMP fusion proteins were constructed that could localize enzyme production in the Golgi apparatus, endosome, ER, mitochondria, or plasma membrane. The fusion proteins significantly increased sAPPη when directed to the endosome, Golgi apparatus, plasma membrane, or mitochondria. Since the C‐terminal region of MT5‐MMP is responsible for its intracellular location and trafficking, this domain was used as the bait in a yeast two‐hybrid screen to identify MT5‐MMP protein partners in a human brain cDNA library. Identified binding partners included N4BP2L1, TMX3, EIG121, bridging Integrator 1 (BIN1), RUFY4, HTRA1, and TMEM199. The binding of N4BP2L1, EIG121, BIN1, or TMX3 to MT5‐MMP resulted in the most significant increase in sAPPη production. Thus, the action of MT5‐MMP on APP occurs in multiple locations within the cell and is facilitated by site‐specific binding partners.

01 Dec 2022·Cancer Cell InternationalQ3 · MEDICINE

As a prognostic biomarker of clear cell renal cell carcinoma RUFY4 predicts immunotherapy responsiveness in a PDL1-related manner

Q3 · MEDICINE

ArticleOA

Author: Miao, Daojia ; Zhang, Xiaoping ; Xiao, Wen ; Xiong, Zhiyong ; Shi, Jian ; Lv, Qingyang ; Meng, Xiangui ; Yang, Hongmei ; Xie, Kairu

AbstractBackgroundClear cell renal cell carcinoma (ccRCC) is one of the most lethal malignancies in the urinary system and the existing immunotherapy has not achieved satisfactory outcomes. Therefore, this study aims at establishing a novel gene signature for immune infiltration and clinical outcome (overall survival and immunotherapy responsiveness) in ccRCC patients.MethodsBased on RNA sequencing data and clinical information in The Cancer Genome Atlas (TCGA) database, we calculated proportions of immune cells in 611 samples using an online tool CIBERSORTx. Multivariate survival analysis was conducted to determine crucial survival-associated immune cells and immune-infiltration-related genes (IIRGs). Next, the clinical specimens and common renal cancer cell lines were applied to confirm IIRGs expression at protein and RNA levels. Finally, functional enrichment analyses and siRNA technology targeted toRUFY4were implemented to verify its function of predicting immunotherapy response.ResultsFollicular helper T cells (TFHs) and Regulatory T cells (Tregs) were highly infiltrated in the tumor microenvironment (TME) and their relative proportions were independent prognostic factors for patients. Among IIRGs of TFHs and TREGs,RUFY4was found to be highly activated in tumor microenvironment and its co-expression network was enriched inPDL1/PD1checkpoint pathway in cancer. Additionally, knockdown ofRUFY4led to the decline ofPDL1and proliferation ability in ccRCC cell lines.ConclusionTFHs and Tregs were considered as prognostic biomarkers andRUFY4was an immunotherapeutic predictor of ccRCC patients in aPDL1-Related manner.

01 Dec 2021·Nutrition & MetabolismQ3 · MEDICINE

Integrative proteomic and lipidomic analysis of Kaili Sour Soup-mediated attenuation of high-fat diet-induced nonalcoholic fatty liver disease in a rat model

Q3 · MEDICINE

ArticleOA

Author: Cheng, Mingliang ; Yu, Lei ; Liu, Yongmei ; Bi, Ying ; Cong, Shuo ; Hu, Yaxin ; Li, Zhengchao

AbstractBackgroundNonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease and is characterized by excessive fat accumulation. Kaili Sour Soup, a food typical of Guizhou Province, is believed to have significant health benefits. Thus, we aimed to identify and assess the impact of Kaili Sour Soup on NAFLD and its underlying mechanism using integrative proteomic and lipidomic analysis.MethodsA high-fat diet and male Wistar rats were used to construct a NAFLD rat model. Haematoxylin and eosin (HE) and Oil Red O staining analyses were used to perform the histologic examination. Proteomic analysis was utilized to systematically identify the global protein profile in NAFLD with and without Kaili Sour Soup treatment. Western blot assays were used to verify the expression of proteins screened by proteomic analysis. Lipidomic analysis was performed to screen lipid metabolism in NAFLD with and without Kaili Sour Soup treatment.ResultsKaili Sour Soup alleviated high-fat diet (HFD)-induced fatty liver and had a normalizing effect on physiological and biochemical indicators of NAFLD, including body weight, liver weight, liver index, total cholesterol (TC), triglyceride (TG), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and insulin resistance level of homeostasis model assessment (HOMA-IR). Kaili Sour Soup decreased the levels of 13 proteins (Tmem44, Rnaseh2b, Gstm6l, LOC100910877, Rufy4, Slc12a2, Pcif1, P4503A1, Sult1e1, Nop53, AABR07065656.4, AABR07065789.3) that were upregulated by HFD and increased the levels of 3 proteins (Sult1c2, Sult1c2a, Snrnp48) that were downregulated by HFD. Kaili Sour Soup attenuated the HFD-induced increase in acyl carnitine (AcCa) and enhanced the HFD-induced decreases in gangliosides (GM3) and lysophosphatidylserine (LPS) in the NAFLD rat model.ConclusionsAltogether, this study revealed that Kaili Sour Soup attenuated HFD-induced fatty liver and systematically identified abnormal proteins and lipids involved in the role of Kaili Sour Soup in a NAFLD rat model.

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