scholarly journals MCP-1 (Monocyte Chemotactic Protein-1)-induced Protein, a Recently Identified Zinc Finger Protein, Induces Adipogenesis in 3T3-L1 Pre-adipocytes without Peroxisome Proliferator-activated Receptor γ

2009 ◽  
Vol 284 (40) ◽  
pp. 27620-27628 ◽  
Author(s):  
Craig W. Younce ◽  
Asim Azfer ◽  
Pappachan E. Kolattukudy
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Protein A ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Monocyte Chemotactic Protein ◽  
Finger Protein ◽  
Chemotactic Protein

Connecting homocysteine and obesity through pyroptosis, gut microbiome, epigenetics, peroxisome proliferator-activated receptor γ, and zinc finger protein 407

2018 ◽  
Vol 96 (10) ◽  
pp. 971-976 ◽  
Author(s):  
Anwesha Laha ◽  
Avisek Majumder ◽  
Mahavir Singh ◽  
Suresh C. Tyagi
Keyword(s):  
Zinc Finger ◽  
Gut Microbiome ◽  
Metabolic Disorders ◽  
Zinc Finger Protein ◽  
Specific Gene ◽  
Peroxisome Proliferator ◽  
Gene Promoters ◽  
Divalent Metal Ions ◽  
Peroxisome Proliferator Activated Receptor ◽  
Finger Protein

Although homocysteine (Hcy), a part of the epigenome, contributes to cell death by pyroptosis and decreases peroxisome proliferator-activated receptor γ (PPARγ) levels, the mechanisms are unclear. Hcy is found in high concentrations in the sera of obese individuals, which can elicit an immune response as well by hypermethylating CpG islands of specific gene promoters, a marker of epigenetics. Hcy has also been established to chelate divalent metal ions like Cu2+ and Zn2+, but this role of Hcy has not been established in relationship with obesity. It has been known for a while that PPARγ dysregulation results in various metabolic disorders including glucose and lipid metabolism. Recently, zinc finger protein 407 (Zfp407) is reported to regulate PPARγ target gene expression without affecting PPARγ transcript and protein levels by synergistically working with PPARγ. However, the mechanism(s) of this synergy, as well as other factors contributing to or inhibiting this synergism, have not been proven. This review suggests that Hcy contributes to pyroptosis, changes gut microbiome, and alters PPARγ-dependent mechanism(s) via Zfp407-mediated upregulated adipogenesis and misbalanced fatty acid metabolism, which can predispose to obesity and, consequently, obesity-related metabolic disorders.

Identification of a Novel Peroxisome Proliferator Responsive cDNA Isolated from Rat Hepatocytes as the Zinc-Finger Protein ZFP-37

1998 ◽  
Vol 152 (1) ◽  
pp. 107-118 ◽  
Author(s):  
John P. Vanden Heuvel ◽  
Peter Holden ◽  
Jonathan Tugwood ◽  
Christine Ingle ◽  
Weiyi Yen ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Rat Hepatocytes ◽  
Peroxisome Proliferator ◽  
Finger Protein

Characterization of the isoforms of MOVO zinc finger protein, a mouse homologue of Drosophila Ovo, as transcription factors

Gene ◽  
2004 ◽  
Vol 336 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Sawako Unezaki ◽  
Mikio Nishizawa ◽  
Emiko Okuda-Ashitaka ◽  
Yasuo Masu ◽  
Masanori Mukai ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Protein A ◽  
Mouse Homologue ◽  
Finger Protein

Functional Analysis of ZNF85 KRAB Zinc Finger Protein, a Member of the Highly Homologous ZNF91 Family

1998 ◽  
Vol 17 (11) ◽  
pp. 931-943 ◽  
Author(s):  
D.A. PONCELET ◽  
E.J. BELLEFROID ◽  
P.V. BASTIAENS ◽  
M.A. DEMOITIÉ ◽  
J.C. MARINE ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Protein A ◽  
Finger Protein

scholarly journals Control of Hepatic Gluconeogenesis by the Promyelocytic Leukemia Zinc Finger Protein

2014 ◽  
Vol 28 (12) ◽  
pp. 1987-1998 ◽  
Author(s):  
Siyu Chen ◽  
Jinchun Qian ◽  
Xiaoli Shi ◽  
Tingting Gao ◽  
Tingming Liang ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Metabolic Diseases ◽  
Zinc Finger Protein ◽  
Promyelocytic Leukemia ◽  
Peroxisome Proliferator ◽  
Hepatic Gluconeogenesis ◽  
Promyelocytic Leukemia Zinc Finger ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatic Glucose ◽  
Glucose Output

The promyelocytic leukemia zinc finger (PLZF) protein is involved in major biological processes including energy metabolism, although its role remains unknown. In this study, we demonstrated that hepatic PLZF expression was induced in fasted or diabetic mice. PLZF promoted gluconeogenic gene expression and hepatic glucose output, leading to hyperglycemia. In contrast, hepatic PLZF knockdown improved glucose homeostasis in db/db mice. Mechanistically, peroxisome proliferator-activated receptor γ coactivator 1α and the glucocorticoid receptor synergistically activated PLZF expression. We conclude that PLZF is a critical regulator of hepatic gluconeogenesis. PLZF manipulation may benefit the treatment of metabolic diseases associated with gluconeogenesis.

scholarly journals Positive Regulation of Apoptosis Signal-regulating Kinase 1 Signaling by ZPR9 Protein, a Zinc Finger Protein

2011 ◽  
Vol 286 (36) ◽  
pp. 31123-31135 ◽  
Author(s):  
Hyun-A Seong ◽  
Haiyoung Jung ◽  
Ravi Manoharan ◽  
Hyunjung Ha
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Protein A ◽  
Positive Regulation ◽  
Finger Protein
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