scholarly journals Mutation of the novel acetylation site at K414R of BECN1 is involved in adipocyte differentiation and lipolysis

2021 ◽  
Author(s):  
Chengqian Li ◽  
Jun Xu ◽  
Qing Yu ◽  
Ping Wang ◽  
Bingzi Dong ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
The Novel ◽  
Acetylation Site

Adipocyte differentiation of 3T3-L1 preadipocytes is dependent on lipoxygenase activity during the initial stages of the differentiation process

2003 ◽  
Vol 375 (3) ◽  
pp. 539-549 ◽  
Author(s):  
Lise MADSEN ◽  
Rasmus K. PETERSEN ◽  
Morten B. SØRENSEN ◽  
Claus JØRGENSEN ◽  
Philip HALLENBORG ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Critical Evaluation ◽  
Nordihydroguaiaretic Acid ◽  
Whole Body ◽  
Transcriptional Networks ◽  
Peroxisome Proliferator ◽  
The Novel ◽  
Differentiation Process ◽  
Peroxisome Proliferator Activated Receptor ◽  
Brown Adipose

Adipocytes play a central role in whole-body energy homoeostasis. Complex regulatory transcriptional networks control adipogensis, with ligand-dependent activation of PPARγ (peroxisome proliferator-activated receptor γ) being a decisive factor. Yet the identity of endogenous ligands promoting adipocyte differentiation has not been established. Here we present a critical evaluation of the role of LOXs (lipoxygenases) during adipocyte differentiation of 3T3-L1 cells. We show that adipocyte differentiation of 3T3-L1 preadipocytes is inhibited by the general LOX inhibitor NDGA (nordihydroguaiaretic acid) and the 12/15-LOX selective inhibitor baicalein. Baicalein-mediated inhibition of adipocyte differentiation was rescued by administration of rosiglitazone. Treatment with baicalein during the first 4 days of the differentiation process prevented adipocyte differentiation; supplementation with rosiglitazone during the same period was sufficient to rescue adipogenesis. Accordingly, we demonstrate that adipogenic conversion of 3T3-L1 cells requires PPARγ ligands only during the first 4 days of the differentiation process. We show that the baicalein-sensitive synthesis of endogenous PPARγ ligand(s) increases rapidly upon induction of differentiation and reaches a maximum on days 3–4 of the adipocyte differentiation programme. The conventional platelet- and leucocyte-type 12(S)-LOXs and the novel eLOX-3 (epidermis-type LOX-3) are expressed in white and brown adipose tissue, whereas only eLOX-3 is clearly expressed in 3T3-L1 cells. We suggest that endogenous PPARγ ligand(s) promoting adipocyte differentiation are generated via a baicalein-sensitive pathway involving the novel eLOX-3.

scholarly journals The Novel Genefad158, Having a Transmembrane Domain and Leucine-rich Repeat, Stimulates Adipocyte Differentiation

2004 ◽  
Vol 279 (33) ◽  
pp. 34840-34848 ◽  
Author(s):  
Kei Tominaga ◽  
Chiharu Kondo ◽  
Takeshi Kagata ◽  
Tomoaki Hishida ◽  
Makoto Nishizuka ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Transmembrane Domain ◽  
The Novel ◽  
Leucine Rich Repeat

scholarly journals Jun Dimerization Protein 2 Controls Senescence and Differentiation via Regulating Histone Modification

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Yu-Chang Huang ◽  
Hitomi Hasegawa ◽  
Shin-Wei Wang ◽  
Chia-Chen Ku ◽  
Ying-Chu Lin ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Dna Sequences ◽  
Adipocyte Differentiation ◽  
Replicative Senescence ◽  
The Novel ◽  
Embryonic Fibroblasts ◽  
Gene Encoding ◽  
Core Histones ◽  
Senescence Program ◽  
Polycomb Repressive Complexes

Transcription factor, Jun dimerization protein 2 (JDP2), binds directly to histones and DNAs and then inhibits the p300-mediated acetylation both of core histones and of reconstituted nucleosomes that contain JDP2 recognition DNA sequences. JDP2 plays a key role as a repressor of adipocyte differentiation by regulation of the expression of the gene C/EBPδ via inhibition of histone acetylation. Moreover, JDP2-deficient mouse embryonic fibroblasts (JDP2−/−MEFs) are resistant to replicative senescence. JDP2 inhibits the recruitment of polycomb repressive complexes (PRC1 and PRC2) to the promoter of the gene encoding p16Ink4a, resulting from the inhibition of methylation of lysine 27 of histone H3 (H3K27). Therefore, it seems that chromatin-remodeling factors, including the PRC complex controlled by JDP2, may be important players in the senescence program. The novel mechanisms that underline the action of JDP2 in inducing cellular senescence and suppressing adipocyte differentiation are reviewed.

scholarly journals The Novel Phosphatidylinositol-3-Kinase (PI3K) Inhibitor Alpelisib Effectively Inhibits Growth of PTEN-Haploinsufficient Lipoma Cells

Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1586 ◽  
Author(s):  
Anna S. Kirstein ◽  
Adrien Augustin ◽  
Melanie Penke ◽  
Michele Cea ◽  
Antje Körner ◽  
...  
Keyword(s):  
Cell Death ◽  
Adipocyte Differentiation ◽  
Suppressor Gene ◽  
Pi3k Inhibitor ◽  
Dependent Manner ◽  
The Novel ◽  
Phosphatidylinositol 3 Kinase ◽  
Akt Phosphorylation ◽  
Ribosomal Protein S6 ◽  
New Treatment

Germline mutations in the tumor suppressor gene PTEN cause PTEN Hamartoma Tumor Syndrome (PHTS). Pediatric patients with PHTS frequently develop lipomas. Treatment attempts with the mTORC1 inhibitor rapamycin were unable to reverse lipoma growth. Recently, lipomas associated with PIK3CA-related overgrowth syndrome were successfully treated with the novel PI3K inhibitor alpelisib. Here, we tested whether alpelisib has growth-restrictive effects and induces cell death in lipoma cells. We used PTEN-haploinsufficient lipoma cells from three patients and treated them with alpelisib alone or in combination with rapamycin. We tested the effect of alpelisib on viability, proliferation, cell death, induction of senescence, adipocyte differentiation, and signaling at 1–100 µM alpelisib. Alpelisib alone or in combination with rapamycin reduced proliferation in a concentration- and time-dependent manner. No cell death but an induction of senescence was detected after alpelisib incubation for 72 h. Alpelisib treatment led to a reduced phosphorylation of AKT, mTOR, and ribosomal protein S6. Rapamycin treatment alone led to increased AKT phosphorylation. This effect could be reversed by combining rapamycin with alpelisib. Alpelisib reduced the size of lipoma spheroids by attenuating adipocyte differentiation. Since alpelisib was well tolerated in first clinical trials, this drug alone or in combination with rapamycin is a potential new treatment option for PHTS-related adipose tissue overgrowth.

The novel steroidal glycoside from the dried bulb of Allium Macrostemon Bunge inhibits platelet activation

2010 ◽  
Vol 34 (8) ◽  
pp. S33-S33
Author(s):  
Wenchao Ou ◽  
Haifeng Chen ◽  
Yun Zhong ◽  
Benrong Liu ◽  
Keji Chen
Keyword(s):  
Platelet Activation ◽  
The Novel ◽  
Steroidal Glycoside ◽  
Allium Macrostemon
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