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33-511: FIAF may refer to: Fasting-Induced Adipose Factor or ANGPTL4, a protein Fédération Internationale des Archives du Film or International Federation of Film Archives, a Paris-based association of film archivists Finnish Air Force Fleet Intelligence Adaptive Force , a U.S. military intelligence unit reporting to Navy Cyber Forces French Institute Alliance Française ,

66-399: A TEK tyrosine kinase antagonist. As a result, the promotion of endothelial activation, destabilization, and inflammation are promoted. Its role during angiogenesis depends on the presence of Vegf-a. Serum levels of angiopoietin-2 expression are associated with the growth of multiple myeloma , angiogenesis, and overall survival in oral squamous cell carcinoma . Circulating angiopoietin-2

99-401: A coiled-coil N-terminal domain and a fibrinogen -like C-terminal domain. In mice, the highest mRNA expression levels of ANGPTL4 are found in white and brown adipose tissue, followed by liver, kidney, muscle and intestinal tissues. Human ANGPTL4 is most highly expressed in the liver as a hepatokine . This gene is induced under hypoxic (low oxygen) condition in various cell types and is

132-439: A matricellular protein to facilitate skin wound healing. ANGPTL4-deficient mice exhibit delayed wound reepithelialization with impaired keratinocyte migration, angiogenesis and altered inflammatory response. ANGPTL4 induces nitric oxide production through an integrin/JAK/STAT3-mediated upregulation of iNOS expression in wound epithelia, and enhances angiogenesis to accelerate wound healing in diabetic mice. ANGPTL4 induces

165-484: A protein that in humans is encoded by the ANGPTL4 gene . Alternatively spliced transcript variants encoded with different isoforms have been described. This gene was previously referred to as ANGPTL2, HFARP, PGAR, or FIAF but has been renamed ANGPTL4. This gene is induced under hypoxic (low oxygen) condition in various cell types and is the target of peroxisome proliferator-activated receptors . The encoded protein

198-647: A New York-based organization for the promotion of Francophone culture La Federación Interamericana de Filatelia , a philatelic organisation for North and South America Topics referred to by the same term [REDACTED] This disambiguation page lists articles associated with the title FIAF . If an internal link led you here, you may wish to change the link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=FIAF&oldid=985248408 " Category : Disambiguation pages Hidden categories: Articles containing French-language text Short description

231-464: A form of programmed cell death induced when contact-dependent cells detach from the surrounding tissue matrix. ANGPTL4 secreted from tumors can bind to integrins , activating downstream signaling and leading to the production of superoxide to promote tumorigenesis . ANGPTL4 disrupts endothelial cell junctions by directly interacting with integrin, VE-cadherin and claudin-5 in a sequential manner to facilitate metastasis . ANGPTL4, specifically

264-468: A greater prospect of the development of septic shock. It has also been shown that imbalances between angiopoietin-1 and angiopoietin-2 signaling can act independently of each other. One angiopoietin factor can signal at high levels while the other angiopoieting factor remains at baseline level signaling. Angiopoietin-2 is produced and stored in Weibel-Palade bodies in endothelial cells and acts as

297-411: A β-catenin-mediated upregulation of ID3 in fibroblasts to reduce scar collagen expression. ANGPTL4 is capable of reversing the fibroblast-to-myofibroblast differentiation induced aligned electrospun fibrous substrates. Cyclic stretching of human tendon fibroblasts stimulated the expression and release of ANGPTL4 protein via TGF-β and HIF-1α signalling, and the released ANGPTL4 was pro-angiogenic. ANGPTL4

330-446: Is a growth factor produced by vascular support cells, specialized pericytes in the kidney, and hepatic stellate cells (ITO) cells in the liver. This growth factor is also a glycoprotein and functions as an agonist for the tyrosine receptor found in endothelial cells. Angiopoietin-1 and tyrosine kinase signaling are essential for regulating blood vessel development and the stability of mature vessels. The expression of Angiopoietin-2 in

363-444: Is a marker for early cardiovascular disease in children on chronic dialysis . Kaposi's sarcoma-associated herpesvirus induces rapid release of angiopoietin-2 from endothelial cells. Angiopoietin-2 is elevated in patients with angiosarcoma . Research has shown angiopoietin signaling to be relevant in treating cancer as well. During tumor growth, pro-angiogenic molecules and anti-angiogenic molecules are off balance. Equilibrium

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396-430: Is a serum hormone directly involved in regulating lipid metabolism. ANGPTL4 plays an important role in numerous cancers and is implicated in the metastatic process by modulating vascular permeability, cancer cell motility and invasiveness. The former name, FIAF, stands for Fasting-Induced Adipose Factor. This gene is a member of the angiopoietin -like gene family and encodes a glycosylated , secreted protein with

429-518: Is also a major factor in vessel stability and maturity. After the physical barrier is removed, under the influence of the growth factors VEGF with addition contributions of other factors like angiopoietin-1, integrins, and chemokines play an essential role. VEGF and ang-1 are involved in endothelial tube formation. Angiopoietin-1 and angiopoietin-2 are modulators of endothelial permeability and barrier function. Endothelial cells secrete angiopoietin-2 for autocrine signaling while parenchymal cells of

462-459: Is also a potent angiogenic factor whose expression is up-regulated in hypoxic retinal Müller cells in vitro and the ischemic retina in vivo. The expression of ANGPTL4 was increased in the aqueous and vitreous of proliferative diabetic retinopathy patients and localized to areas of retinal neovascularization. ANGPTL4 has been established as a potent inhibitor of serum triglyceride (TG) clearance, causing elevation of serum TG levels via inhibition of

495-455: Is critical for vessel maturation, adhesion, migration, and survival. Angiopoietin-2, on the other hand, promotes cell death and disrupts vascularization. Yet, when it is in conjunction with vascular endothelial growth factors, or VEGF , it can promote neo-vascularization. Structurally, angiopoietins have an N-terminal super clustering domain, a central coiled domain, a linker region, and a C-terminal fibrinogen-related domain responsible for

528-399: Is different from Wikidata All article disambiguation pages All disambiguation pages Fasting-Induced Adipose Factor 6EUB , 6U0A , 6U1U , 6U73 51129 57875 ENSG00000167772 ENSMUSG00000002289 Q9BY76 Q9Z1P8 NM_001039667 NM_016109 NM_139314 NM_020581 NP_001034756 NP_647475 NP_065606 Angiopoietin-like 4 is

561-459: Is highly contested, it is clear that TIE-2 is capable of activation as a result of binding angiopoietins. Angiopoietin proteins 1 through 4 are all ligands for Tie-2 receptors. Tie-1 heterodimerizes with Tie-2 to enhance and modulate signal transduction of Tie-2 for vascular development and maturation. These Tyrosine kinase receptors are typically expressed on vascular endothelial cells and specific macrophages for immune responses. Angiopoietin-1

594-412: Is more highly induced in nonexercising muscle than in exercising human muscle during acute exercise. ANGPTL4 in nonexercising muscle presumably leads to reduced local uptake of plasma triglyceride-derived fatty acids and their sparing for use by exercising muscle. The induction of ANGPTL4 in exercising muscle likely is counteracted via AMP-activated protein kinase (AMPK)-mediated down-regulation, promoting

627-534: Is not present. Ang-2 works with VEGF to facilitate cell proliferation and migration of endothelial cells. Changes in expression of Ang-1, Ang-2 and VEGF have been reported in the rat brain after cerebral ischemia. To migrate, the endothelial cells need to loosen the endothelial connections by breaking down the basal lamina and the ECM scaffold of blood vessels. These connections are a key determinant of vascular permeability and relieve peri-endothelial cell contact, which

660-602: The C-terminal fragment (cANGPTL4), is a key player that coordinates an increase in cellular energy flux crucial for epithelial-mesenchymal transition (EMT) via an ANGPTL4:YWHAG (14-3-3γ) signaling axis. The ANGPTL4:YWHAG signaling axis confers metabolic flexibility and enhances EMT competency through interaction with specific phosphorylation signals on target proteins. A direct consequence is that ANGPTL4 secures ample cellular energy to fuel multiple ABC transporters to confer EMT-mediated chemoresistance. ANGPTL4 functions as

693-467: The absence of vascular endothelial growth factor (VEGF) leads to endothelial cell death and vascular regression. Increased levels of Ang2 promote tumor angiogenesis, metastasis , and inflammation. Effective means to control Ang2 in inflammation and cancer should have clinical value. Angiopoeitin, more specifically Ang-1 and Ang-2, work hand in hand with VEGF to mediate angiogenesis. Ang-2 works as an antagonist of Ang-1 and promotes vessel regression if VEGF

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726-491: The binding and activation of downstream intracellular enzymes , a process known as cell signaling. Tie-2/Ang-1 signaling activates β1- integrin and N- cadherin in LSK-Tie2+ cells and promotes hematopoietic stem cell (HSC) interactions with extracellular matrix and its cellular components. Ang-1 promotes quiescence of HSC in vivo. This quiescence or slow cell cycling of HSCs induced by Tie-2/Ang-1 signaling contributes to

759-427: The binding between the ligand and receptor. Angiopoietin-1 encodes a 498 amino acid polypeptide with a molecular weight of 57 kDa whereas angiopoietin-2 encodes a 496 amino acid polypeptide. Angiopoietin-1 and angiopoietin-2 can form dimers, trimers, and tetramers. Angiopoietin-1 has the ability to form higher order multimers through its super clustering domain. However, not all of the structures can interact with

792-461: The enzyme lipoprotein lipase (LPL). Biochemical studies indicate that ANGPTL4 disables LPL partly by dissociating the catalytically active LPL dimer into inactive LPL monomers. However, evidence also suggests that ANGPTL4 functions as a conventional, non-competitive inhibitor that binds to LPL to prevent the hydrolysis of substrate as part of reversible mechanism. As a consequence, ANGPTL4 knockout mice have reduced serum triglyceride levels, whereas

825-642: The extravascular tissue secrete angiopoietin-2 onto endothelial cells for paracrine signaling , which then binds to the extracellular matrix and is stored within the endothelial cells. Angiopoietin-2 has been proposed as a biomarker in different cancer types. Angiopoietin-2 expression levels are proportional to the cancer stage for both small and non-small cell lung cancers. It has been also implicated to play role in hepatocellular and endometrial carcinoma-induced angiogenesis. Experiments using blocking antibodies for angiopoietin-2 have shown to decrease metastasis to lungs and lymph nodes. Deregulation of angiopoietin and

858-639: The infection compared to wild-type mice. The treatment of infected mice with neutralizing anti-ANGPTL4 antibodies significantly accelerated pulmonary recovery and improved lung tissue integrity. It was also shown that antibody treatment against ANGPTL4 reduces pulmonary edema and injury in secondary pneumococcal pneumonia . Angiopoietin In addition, there are a number of proteins that are closely related to ('like') angiopoietins ( Angiopoietin-related protein 1 , ANGPTL2 , ANGPTL3 , ANGPTL4 , ANGPTL5 , ANGPTL6 , ANGPTL7 , ANGPTL8 ). Angiopoietin-1

891-505: The maintenance of long-term repopulating ability of HSC and the protection of the HSC compartment from various cellular stresses. Tie-2/Ang-1 signaling plays a critical role in the HSC that is required for the long-term maintenance and survival of HSC in bone marrow. In the endosteum , Tie-2/Ang-1 signaling is predominantly expressed by osteoblastic cells. Although which specific TIE receptors mediate signals downstream of angiogenesis stimulation

924-479: The monomeric C-terminal portion of ANGPTL4 (cANGPTL4). The nANGPTL4 and cANGPTL4 have different biological functions. Monoclonal antibodies targeting the nANGPTL4 and cANGPTL4 have been developed to distinguish their functions. ANGPTL4 plays an important role in numerous cancers and is implicated in the metastatic process by modulating vascular permeability, cancer cell motility and invasiveness. ANGPTL4 contributes to tumor growth and protects cells from anoikis ,

957-462: The opposite is true for mice over-expressing ANGPTL4. ANGPTL4 suppresses foam cell formation to reduce atherosclerosis development. The reduction in LPL activity in adipose tissue during fasting is likely caused by increased local production of ANGPTL4. In other tissues such as heart, production of ANGPTL4 is stimulated by fatty acids and may serve to protect cells against excess fat uptake. ANGPTL4

990-426: The target of peroxisome proliferator-activated receptors . The encoded protein is a serum hormone directly involved in regulating lipid metabolism. The native full length ANGPTL4 can form higher order structures via intermolecular disulfide bonds. The N-terminal region of ANGPTL4 (nANGPTL4) is responsible for its assembly. The full length ANGPTL4 undergoes proteolytic cleavage at the linker region, releasing nANGPTL4 and

1023-471: The tyrosine kinase pathway is common in blood-related diseases such as diabetes , malaria , sepsis , and pulmonary hypertension . This is demonstrated by an increased ratio of angiopoietin-2 and angiopoietin-1 in blood serum. To be specific, angiopoietin levels provide an indication for sepsis . Research on angiopoietin-2 has shown that it is involved in the onset of septic shock. The combination of fever and high levels of angiopoietin-2 are correlated with

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1056-460: The tyrosine kinase receptor. The receptor can only be activated at the tetramer level or higher. The collective interactions between angiopoietins, receptor tyrosine kinases , vascular endothelial growth factors and their receptors form the two signaling pathways— Tie-1 and Tie-2 . The two receptor pathways are named as a result of their role in mediating cell signals by inducing the phosphorylation of specific tyrosines. This in turn initiates

1089-538: The use of plasma triglycerides as fuel for active muscles. High-throughput RNA sequencing of lung tissue samples from the 1918 and 2009 influenza pandemic revealed that ANGPTL4 was one of the most significantly upregulated gene. Murine influenza infection of the lungs stimulated the expression of ANGPTL4 via a STAT3-mediated mechanism. ANGPTL4 enhanced pulmonary tissue leakiness and exacerbated inflammation-induced lung damage. Influenza-infected ANGPTL4-knockout mice displayed diminished lung damage and recovered faster from

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