scholarly journals PERAN LATIHAN FISIK DALAM PENANGANAN OBESITAS: AKSI IRISIN PADA PROSES PENCOKELATAN

2021 ◽  
Vol 3 (1) ◽  
pp. 27
Author(s):  
Dewi Irawati Soeria Santoso ◽  
Imelda Rosalyn Sianipar ◽  
Neng Tine Kartinah
Keyword(s):  
Treatment Approach ◽  
Public Health Problem ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Brown Adipocyte ◽  
White Adipocyte ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Prevalence Of Obesity

In recent years, the prevalence of obesity continues to increase, leading to a public health problem. Therefore, the obesity problem needs serious attention and treatment approaches. Exercise is one of the treatment approach to combat obesity because exercise plays a role in beiging/browning process. Beiging is a differentiation process from white adipocyte to beige adipocyte, which has similar characteristics to brown adipocyte and is marked with an increase of UCP-1 expression. Irisin plays a role in increasing UCP-1 expression by activating p38 mitogen-activated protein kinase (MAPK) and extracellular-signal regulated kinase (ERK) signaling. Muscle contraction during exercise can activate PGC-1α, which leads to the synthesis of irisin. Exercise may increase irisin levels in skeletal muscle and consequently, play as a mediator of beiging process in adipose tissue.

PERAN LATIHAN FISIK DALAM PENANGANAN OBESITAS: AKSI IRISIN PADA PROSES PENCOKELATAN

2019 ◽  
Vol 1 (1) ◽  
pp. 26
Author(s):  
Dewi Irawati Soeria Santoso ◽  
Rabia Rabia ◽  
Imelda Rosalyn Sianipar ◽  
Neng Tine Kartinah
Keyword(s):  
Treatment Approach ◽  
Public Health Problem ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Brown Adipocyte ◽  
White Adipocyte ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Prevalence Of Obesity

In recent years, the prevalence of obesity continues to increase, leading to a public health problem. Therefore, the obesity problem needs serious attention and treatment approaches. Exercise is one of the treatment approach to combat obesity because exercise plays a role in beiging/browning process. Beiging is a differentiation process from white adipocyte to beige adipocyte, which has similar characteristics to brown adipocyte and is marked with an increase of UCP-1 expression. Irisin plays a role in increasing UCP-1 expression by activating p38 mitogen-activated protein kinase (MAPK) and extracellular-signal regulated kinase (ERK) signaling. Muscle contraction during exercise can activate PGC-1?, which leads to the synthesis of irisin. Exercise may increase irisin levels in skeletal muscle and consequently, play as a mediator of beiging process in adipose tissue.

scholarly journals Extracellular Signal-regulated Kinase Regulates Clathrin-independent Endosomal Trafficking

2006 ◽  
Vol 17 (2) ◽  
pp. 645-657 ◽  
Author(s):  
Sarah E. Robertson ◽  
Subba Rao Gangi Setty ◽  
Anand Sitaram ◽  
Michael S. Marks ◽  
Robert E. Lewis ◽  
...  
Keyword(s):  
Surface Expression ◽  
Mek Inhibitor ◽  
Endocytic Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Endosomal Trafficking ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Kinase Suppressor Of Ras ◽  
Mitogen Activated Protein

Extracellular signal-regulated kinase (Erk) is widely recognized for its central role in cell proliferation and motility. Although previous work has shown that Erk is localized at endosomal compartments, no role for Erk in regulating endosomal trafficking has been demonstrated. Here, we report that Erk signaling regulates trafficking through the clathrin-independent, ADP-ribosylation factor 6 (Arf6) GTPase-regulated endosomal pathway. Inactivation of Erk induced by a variety of methods leads to a dramatic expansion of the Arf6 endosomal recycling compartment, and intracellular accumulation of cargo, such as class I major histocompatibility complex, within the expanded endosome. Treatment of cells with the mitogen-activated protein kinase kinase (MEK) inhibitor U0126 reduces surface expression of MHCI without affecting its rate of endocytosis, suggesting that inactivation of Erk perturbs recycling. Furthermore, under conditions where Erk activity is inhibited, a large cohort of Erk, MEK, and the Erk scaffold kinase suppressor of Ras 1 accumulates at the Arf6 recycling compartment. The requirement for Erk was highly specific for this endocytic pathway, because its inhibition had no effect on trafficking of cargo of the classical clathrin-dependent pathway. These studies reveal a previously unappreciated link of Erk signaling to organelle dynamics and endosomal trafficking.

scholarly journals Extracellular Signal-Regulated Kinase Promotes Rho-Dependent Focal Adhesion Formation by Suppressing p190A RhoGAP

2010 ◽  
Vol 30 (13) ◽  
pp. 3233-3248 ◽  
Author(s):  
Ashok K. Pullikuth ◽  
Andrew D. Catling
Keyword(s):  
Adhesion Formation ◽  
Rho Kinase ◽  
Focal Adhesions ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Extracellular Signal Regulated Kinase ◽  
Erk Phosphorylation ◽  
C Terminus ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

ABSTRACT Cell migration is critical for normal development and for pathological processes including cancer cell metastasis. Dynamic remodeling of focal adhesions and the actin cytoskeleton are crucial determinants of cell motility. The Rho family and the mitogen-activated protein kinase (MAPK) module consisting of MEK-extracellular signal-regulated kinase (ERK) are important regulators of these processes, but mechanisms for the integration of these signals during spreading and motility are incompletely understood. Here we show that ERK activity is required for fibronectin-stimulated Rho-GTP loading, Rho-kinase function, and the maturation of focal adhesions in spreading cells. We identify p190A RhoGAP as a major target for ERK signaling in adhesion assembly and identify roles for ERK phosphorylation of the C terminus in p190A localization and activity. These observations reveal a novel role for ERK signaling in adhesion assembly in addition to its established role in adhesion disassembly.

scholarly journals Mitogen-activated protein kinase (MAPK) blockade of bovine preimplantation embryogenesis requires inhibition of both p38 and extracellular signal-regulated kinase (ERK) pathways

Reproduction ◽  
2005 ◽  
Vol 130 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Pavneesh Madan ◽  
Michele D Calder ◽  
Andrew J Watson
Keyword(s):  
P38 Mapk ◽  
Mapk Signaling ◽  
Blastocyst Stage ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Bovine Embryos ◽  
Blastocyst Formation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Blastocyst formation, as a critical period during development, is an effective indicator of embryonic health and reproductive efficiency. Out of a number of mechanisms underlying blastocyst formation, highly conserved mitogen-activated protein kinase (MAPK) signaling has emerged as a major mechanism involved in regulating murine preimplantation embryo development. The objective of our study was to ascertain the role of MAPK signaling in regulating bovine development to the blastocyst stage. Using reverse transcriptase PCR and immunohistochemical staining procedures we have demonstrated that mRNA transcripts and polypeptides encoding p38 MAPK pathway constituents are detectable in preimplantation bovine embryos from the one-cell to the blastocyst stage. Further, the effects on bovine embryo development following inhibition of p38 α/β and extracellular signal-regulated kinase (ERK) signaling by treatment with SB220025 and U0126, respectively, were investigated. Eight-cell bovine embryos (50 per group; three replicates) were placed into treatments consisting of synthetic oviductal fluid (SOF) medium: SOF + SB202474 (inactive analogue), SOF + SB220025, SOF + U0124 (inactive analogue), SOF + U0126, and SOF + SB220025 + U0126. Inhibition of p38 MAPK or ERK signaling individually did not affect development to the blastocyst stage. However, when both pathways were blocked simultaneously there was a significant reduction (P< 0.05) in blastocyst formation, cell number and immunofluorescence of phosphorylated downstream pathway constituents. We have determined that, in variance to what was observed during murine preimplantation development, bovine early embryos progress at normal frequencies to the blastocyst stage in the presence of p38 MAPK inhibitors.

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