aggregation

Platelet endothelial aggregation receptor-1 (PEAR1), an epidermal growth factor repeat-containing transmembrane receptor, is known to participate in platelet contact-induced activation. Platelet endothelial aggregation receptor 1 (PEAR1) triggers platelet aggregation and is expressed in platelets and endothelial cells.PEAR1 encodes the Platelet-Endothelial Aggregation Receptor 1, a contact receptor involved in platelet function and megakaryocyte and endothelial cell proliferation. PEAR1 expression during megakaryocyte differentiation is controlled by DNA methylation at its first CpG island.

Inhibits fibrinogen interaction with platelets. Acts by binding to the glycoprotein IIb-IIIa receptor (ITGA2B ITGB3) on the platelet surface and inhibits aggregation induced by ADP, thrombin, platelet-activating factor and collagen. Also inhibits T24 and SK-Mel-28 cell adhesion to fibronectin with IC(50) of 4.4 uM and 33 nM, respectively. Disintegrin batroxostatin Protein, Bothrops atrox, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 15.2 kDa and the accession number is P18618.

Serum amyloid A-2 protein (SAA2) belongs to the SAA family. It expressed by the liver and secreted in plasma. SAA2 functions as major acute phase reactant and could works as apolipoprotein of the HDL complex. Increased levels of A-SAA in serum are indicative of inflammatory disease. When highly expressed, SAA can displace ApoA1 as the major apolipoprotein in HDL complexes, weakening the function of HDL as a reverse (lipid clearing) cholesterol transporter. A highly charged region of SAA2 and SAA1 (aa 36-68) contains putative fibronectin- and laminin-binding motifs. This region also binds heparin sulfate proteoglycans at mildly acidic pH and promotes aggregation of A-SAA.

Metalloproteinase that binds to von Willebrand factor (VWF) and induces its interaction with GPIb (GP1BA), resulting in platelet aggregation. SVMP Protein, Bothrops jararaca, Recombinant (His & KSI) is expressed in E. coli expression system with N-6xHis-KSI tag. The predicted molecular weight is 18.0 kDa and the accession number is P22028.

Acts as an intracellular estrogen-binding protein. May be involved in modulating cellular levels and biological functions of estrogens in the pancreas. May act as a chaperone that inhibits aggregation of misfolded proteins.

Protects DNA from oxidative damage by sequestering intracellular Fe(2+) ion and storing it in the form of Fe(3+) oxyhydroxide mineral. One hydrogen peroxide oxidizes two Fe(2+) ions, which prevents hydroxyl radical production by the Fenton reaction. It protects DNA from hydroxyl radical-mediated cleavage. Binds DNA with no apparent sequence specificity without self-aggregation nor promotion of DNA condensation. Is unable to protect DNA from DNase-mediated cleavage. Dps Protein, Mycobacterium smegmatis, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 36.3 kDa and the accession number is P0C558.

Released during platelet aggregation. Neutralizes the anticoagulant effect of heparin because it binds more strongly to heparin than to the chondroitin-4-sulfate chains of the carrier molecule. Chemotactic for neutrophils and monocytes. Inhibits endothelial cell proliferation. CXCL4 Protein, Pig, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 17.1 kDa and the accession number is P30034.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

The growth arrest-specific 6 gene (GAS6) is a member of the family of plasma vitamin K-dependent proteins, which are able to bind to phospholipids using an N-terminal gamma-carboxyglutamic acid domain. GAS6 is a vitamin K-dependent protein, plays a role in the survival, proliferation, migration, differentiation, adhesion, and apoptosis of cells. The growth arrest-specific 6 (GAS6) has been implicated in systemic inflammation and coagulation. Growth arrest-specific 6 (GAS6), plays a role in tumor progression by regulating growth in many cancers. GAS6, expressed by osteoblasts in the bone marrow, plays a significant role in the regulation of PCa cell survival during chemotherapy, which will have important implications for targeting metastatic disease. The GAS6 TYRO3-AXL-MERTK (TAM) signaling pathway is essential for full and sustained platelet activation, as well as thrombus stabilization. Inhibition of this pathway decreases platelet aggregation, shape change, clot retraction, aggregate formation under flow conditions, and surface expression of activation markers. It had been show that GAS6 signaling regulates invasion, proliferation, chemotherapy-induced apoptosis of prostate cancer (PCa) cells, and GAS6 secreted from osteoblasts in the bone marrow environment plays a critical role in establishing prostate tumor cell dormancy.

Fcgr4, also known as CD16-2, is one of the receptors for Fc region of IgG which involve in immune responses. Fcgr4 mainly functions in cellular response to lipopolysaccharide, NK T cell proliferation, regulation of sensory perception of pain, wound healing etc. Three groups are included for Fc γ receptors (FcR), and they are Fc γ RI (CD64), Fc γ RII (CD32), and Fc γ RIII (CD16). Among these, CD64 possess high affinity even for monomeric IgG, while CD32 and CD16 display a relative lower affinity for IgG. Genes encodes these receptors are diverse differing by species and cell types. The aggregation of FcR having immunoreceptor tyrosine-based activation motifs (ITAMs) activates sequentially src family tyrosine kinases and syk family tyrosine kinases that connect transduced signals to common activation pathways shared with other receptors. FcR with ITAMs elicit cell activation, endocytosis, and phagocytosis. Fcgr4 belongs to Fc γ RIII (CD16) group.

Alpha-Crystallin A Chain (CRYAA) belongs to the small heat shock protein (HSP20) family and can be induced by heat shock. The expression of CRYAA is preferentially restricted to the lens cell. CRYAA may contribute to the transparency and refractive index of the lens. CRYAA has chaperone-like activity, preventing aggregation of various proteins under a wide range of stress conditions. Two additional functions of CRYAA are an autokinase activity and participation in the intracellular architecture.

Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST GP130, IL27RA WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2 FPRL1 and FPR3 FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6 APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2 FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.

Production of extracellular glucans, that are thought to play a key role in the development of the dental plaque because of their ability to adhere to smooth surfaces and mediate the aggregation of bacterial cells and food debris. Glucosyltransferase-SI Protein, S. mutans serotype c, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 26.7 kDa and the accession number is P13470.

Histones are a complex family of highly conserved basic proteins responsible for packaging chromosomal DNA into nucleosomes. There are subtype diversities: H1, H2A, H2B, and H3 or H4. It has become more and more evident that histone modifications are key players in the regulation of chromatin states and dynamics as well as in gene expression. Therefore, histone modifications and the enzymatic machinery that set them are crucial regulators that can control cellular proliferation, differentiation, plasticity, and malignancy processes. However, extracellular histones are a double-edged sword because they also damage host tissue and may cause death. Histones bound to platelets, induced calcium influx, and recruited plasma adhesion proteins such as fibrinogen to induce platelet aggregation. Histone cluster 3, H2a also known as histone H2A (HIST3H2A) is a member of histones. Covalent modification of histones is important in regulating chromatin dynamics and transcription. One example of such modification is ubiquitination, which mainly occurs on histones H2A and H2B. E3 ubiquitin ligase complex is specific for histone H2A (HIST3H2A). Reducing the expression of Ring2 results in a dramatic decrease in the level of ubiquitinated H2A in HeLa cells. DNA damage induces monoubiquitylation of histone H2A (HIST3H2A) in the vicinity of DNA lesions.

Cofilin 2 (muscle), also known as CFL2, is a member of cofilin family of the actin-binding protein superfamily. Cofilin2 shows significant homology to the other two members: cofilin 1 and DSTN, through its entire sequence, and contains residues conserved among the cofilin family that are responsible for actin-binding. Cofilin 2 (CFL2) is an important regulator of striated myocyte function. Purified cofilin 2 depolymerized actin filaments in a dose- and pH-dependent manner and reduced the apparent viscosity of an actin solution, although they did not co-sediment with actin filaments at all. Cofilin2 is not expressed in vegetative cells, but is transiently induced during the aggregation stage of development, whereas cofilin 1 was predominantly expressed in vegetative cells.

Muscle, skeletal receptor tyrosine-protein kinase, also known as Muscle-specific tyrosine-protein kinase receptor, Muscle-specific kinase receptor, and MUSK, is a single-pass type I membrane protein that belongs to the protein kinase superfamily and tyr protein kinase family. MUSK contains one FZ (frizzled) domain, three Ig-like C2-type (immunoglobulin-like) domains, and one protein kinase domain. This protein is a muscle-specific tyrosine kinase receptor and it may play a role in clustering of the acetylcholine receptor in the postsynaptic neuromuscular junction. MUSK expression is increased in muscle cells stimulated with Wnt or at conditions when the Wnt signaling was activated. MUSK is a muscle-specific receptor tyrosine kinase that is activated by agrin. It has a critical role in neuromuscular synapse formation. MUSK is a receptor tyrosine kinase that is a key mediator of agrin's action and is involved in neuromuscular junction (NMJ) organization. Defects in the MUSK encoding gene are a cause of autosomal recessive congenital myasthenic syndrome (CMS). Congenital myasthenic syndromes are inherited disorders of neuromuscular transmission that stem from mutations in presynaptic, synaptic, or postsynaptic proteins. MUSK mutations lead to decreased agrin-dependent AChR aggregation, a critical step in the formation of the neuromuscular junction. Mutations in this receptor encoding gene also have been associated with the congenital myasthenic syndrome.

Podoplanin is a type-1 transmembrane protein that belongs to Podoplanin family. PDPN expressed in various specialized cell types throughout the body. It highly expressed in placenta, lung, skeletal muscle and brain, weakly expressed in brain, kidney and liver. In placenta, PDPN expressed on the apical plasma membrane of endothelium, in lung, expressed in alveolar epithelium. PDPN physiological function is related to its mucin-type character. PDPN may be involved in cell migration and or actin cytoskeleton organization. When expressed in keratinocytes, induces changes in cell morphology with transfected cells showing an elongated shape, numerous membrane protrusions, and major reorganization of the actin cytoskeleton, increased motility and decreased cell adhesion. It requires for normal lung cell proliferation and alveolus formation at birth and Induces platelet aggregation. Nevertheless, it doesn’t have any effect on amino acid transport and the aquaporin-type water channels.

Glycoprotein VI (GPVI) is a 63 kDa platelet megakaryocyte-specific type I transmembrane glycoprotein of the immunoglobulin superfamily that is an important collagen receptor and initiator of platelet activation, aggregation and thrombin generation. GPVI is also a secondary receptor required for platelet spreading on laminin. GPVI associates with the Fc receptor gamma -chain via charged aa in the TM domains of GPVI (arginine) and the FcR gamma (aspartic acid). Collagen binding by the GPVI Ig-like domains initiates signaling through the FcR gamma ITAM sequence. Dimerization of GPVI (2:2 with FcR gamma ) and N-glycosylation greatly enhances collagen binding. Type I and III collagens are strong thrombus-forming components in the vascular subendothelium and atherosclerotic plaques. GPVI initiates binding to fibrillar collagens under flow conditions, then activates integrin alpha 2 beta 1 which binds collagen more tightly. GPVI deficiencies cause only a mild bleeding tendency, probably because integrin alpha 2 beta 1 is able to minimally initiate collagen binding. Normal human GPVI concentration can vary widely and affect maximum thrombin generation. Engagement of GPVI by collagens or other agonists, including autoantibodies, causes calmodulin-regulated metalloproteinase cleavage of the 57 kDa ECD and depletes surface GPVI.

Kininogen-1 is a secreted protein which contains three cystatin domains. There are two alternatively spliced forms, designated as the high molecular weight (HMW) and low MW (LMW) forms. Kininogen-1 plays a critical role in blood coagulation and inflammatory response. Kininogens are inhibitors of thiol proteases. Kininogen-1 participates in blood coagulation by helping to position optimally prekallikrein and factor XI next to factor XII, also inhibits the thrombin- and plasmin-induced aggregation of thrombocytes. The active peptide bradykinin that is released from Kininogen-1 shows a variety of physiological effects: influence in smooth muscle contraction, induction of hypotension, natriuresis and diuresis, decrease in blood glucose level. It is a mediator of inflammation and causes increase in vascular permeability, stimulation of nociceptors release of other mediators of inflammation. It has a cardioprotective effect. LMW-kininogen inhibits the aggregation of thrombocytes and doesn’t involved in blood clotting.

Elicits platelet aggregation by the binding to the C-type lectin domain family 1 member B (CLEC1B CLEC2). Binding leads to tyrosine phosphorylation in the cytoplasmic tail of CLEC1B, which promotes the binding of spleen tyrosine kinase (Syk), subsequent activation of PLC-gamma-2, and platelet activation and aggregation. Binding to GPIbalpha (GP1BA) and alpha-2 beta-1 (ITGA2 ITGB1) may also induce aggregation, but this is controversial. Snaclec rhodocytin subunit alpha Protein, Calloselasma rhodostoma, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 31.8 kDa and the accession number is Q9I841.

Elicits platelet aggregation by the binding to the C-type lectin domain family 1 member B (CLEC1B CLEC2). Binding leads to tyrosine phosphorylation in the cytoplasmic tail of CLEC1B, which promotes the binding of spleen tyrosine kinase (Syk), subsequent activation of PLCgamma2, and platelet activation and aggregation. Binding to GPIbalpha (GP1BA) and alpha2 beta-1 (ITGA2 ITGB1) may also induce aggregation, but this is controversial. Snaclec rhodocytin subunit beta Protein, Calloselasma rhodostoma, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 16.4 kDa and the accession number is Q9I840.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

OFPSparkTM is a red (orange) fluorescent protein (excitation emission maxima are 549 and 566 nm, respectively) derived from DsRed. Possessing high photostability and pH stability, OFPSparkTM is more than twice brighter than mOrange2. Fast OFPSparkTM maturation makes it detectable in mammalian cells as early as within 8 hrs after transfection. OFPSparkTM can be expressed and detected in a wide range of organisms. Mammalian cells transiently transfected with OFPSparkTM expression vectors produce bright fluorescence in 8 hrs after transfection. No cytotoxic effects or visible protein aggregation are observed. For its monomer structure, OFPSparkTM performs well in some fusions and protein labeling applications.

DnaJ Homolog Subfamily B Member 1 (DNAJB1) is a member of the heat shock protein family. Heat shock proteins (HSPs) are a highly conserved family of stress response proteins. HSPs function primarily as molecular chaperones, facilitating the folding of other cellular proteins, preventing protein aggregation, or targeting improperly folded proteins to specific degradative pathways. DNAJB1 regulates cellular processes by aiding in the folding, transport and assembly. DNAJB1 contains a J-domain which controls interaction with the ATPase domain of DnaK. DNAJB1 interacts with HSP70 and can stimulate its ATPase activity. In addition, DNAJB1 stimulates the association between HSC70 and HIP.

Thrombin-like snake venom serine protease that clots fibrinogen by releasing fibrinopeptide A from the alpha chain of fibrinogen (FGA), induces platelet aggregation through its interaction with GPIb (GP1BA GP1BB), and activates factor VIII (F8). SVTLE Protein, Bothrops jararaca, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 33.0 kDa and the accession number is P81661.

Non-hemorrhagic metalloproteinase that hydrolyzes the alpha chains of fibrinogen, as well as fibrin, fibronectin and casein. Beta and gamma chains are also hydrolyzed, but more slowly. Thrombolytic activity is also observed. Induces detachment of endothelial cells followed by death, and inhibits endothelial cell adhesion to fibronectin. Induces edema in mouse paw. Inhibits ADP-induced platelet aggregation on human platelet-rich plasma with an IC(50) of 2.8 uM. SVMP Protein, Bothrops leucurus, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 30.5 kDa and the accession number is P84907.

Virulence factor that contributes to intimate adherence of enterohemorrhagic E.coli (EHEC) O157:H7 to host cells. Is able to cleave the secreted human mucin 7 (MUC7) and the glycoprotein 340 (DMBT1 GP340). Also cleaves human C1 inhibitor (SERPING1), a regulator of multiple inflammatory pathways, and binds and localizes it to bacterial and host cell surfaces, protecting them from complement-mediated lysis. Therefore, the current model proposes two roles for StcE during infection: it acts first as a mucinase, allowing passage of EHEC through the oral cavity by cleaving the salivary glycoproteins that are responsible for bacterial aggregation. Similarly, in the colon, StcE cleaves the glycoproteins that protect the intestinal epithelial surface, allowing EHEC to come into close contact with host cell membranes. Secondly, it acts as an anti-inflammatory agent by localizing SERPING1 to cell membranes.

Plays a role as a neuroprotective factor. Protects against neuronal cell death induced by multiple different familial Alzheimer disease genes and amyloid-beta proteins in Alzheimer disease. Mediates its neuroprotective effect by interacting with a receptor complex composed of IL6ST GP130, IL27RA WSX1 and CNTFR. Also acts as a ligand for G-protein coupled receptors FPR2 FPRL1 and FPR3 FPRL2. Inhibits amyloid-beta protein 40 fibril formation. Also inhibits amyloid-beta protein 42 fibril formation. Suppresses apoptosis by binding to BAX and preventing the translocation of BAX from the cytosol to mitochondria. Also suppresses apoptosis by binding to BID and inhibiting the interaction of BID with BAX and BAK which prevents oligomerization of BAX and BAK and suppresses release of apoptogenic proteins from mitochondria. Forms fibers with BAX and also with BID, inducing BAX and BID conformational changes and sequestering them into the fibers which prevents their activation. Can also suppress apoptosis by interacting with BIM isoform BimEL, inhibiting BimEL-induced activation of BAX, blocking oligomerization of BAX and BAK, and preventing release of apoptogenic proteins from mitochondria. Plays a role in up-regulation of anti-apoptotic protein BIRC6 APOLLON, leading to inhibition of neuronal cell death. Binds to IGFBP3 and specifically blocks IGFBP3-induced cell death. Competes with importin KPNB1 for binding to IGFBP3 which is likely to block IGFBP3 nuclear import. Induces chemotaxis of mononuclear phagocytes via FPR2 FPRL1. Reduces aggregation and fibrillary formation by suppressing the effect of APP on mononuclear phagocytes and acts by competitively inhibiting the access of FPR2 to APP. Protects retinal pigment epithelium (RPE) cells against oxidative stress-induced and endoplasmic reticulum (ER) stress-induced apoptosis. Promotes mitochondrial biogenesis in RPE cells following oxidative stress and promotes STAT3 phosphorylation which leads to inhibition of CASP3 release. Also reduces CASP4 levels in RPE cells, suppresses ER stress-induced mitochondrial superoxide production and plays a role in up-regulation of mitochondrial glutathione. Reduces testicular hormone deprivation-induced apoptosis of germ cells at the nonandrogen-sensitive stages of the seminiferous epithelium cycle. Protects endothelial cells against free fatty acid-induced inflammation by suppressing oxidative stress, reducing expression of TXNIP and inhibiting activation of the NLRP3 inflammasome which inhibits expression of proinflammatory cytokines IL1B and IL18. Protects against high glucose-induced endothelial cell dysfunction by mediating activation of ERK5 which leads to increased expression of transcription factor KLF2 and prevents monocyte adhesion to endothelial cells. Inhibits the inflammatory response in astrocytes. Increases the expression of PPARGC1A PGC1A in pancreatic beta cells which promotes mitochondrial biogenesis. Increases insulin sensitivity.

Key enzyme in the cholesterol biosynthesis pathway. Catalyzes the cyclization of (S)-2,3 oxidosqualene to lanosterol, a reaction that forms the sterol nucleus. Through the production of lanosterol may regulate lens protein aggregation and increase transparency.

Integral membrane protein associated with integrins, which regulates different processes, such as sperm-egg fusion, platelet activation and aggregation, and cell adhesion. Present at the cell surface of oocytes and plays a key role in sperm-egg fusion, possibly by organizing multiprotein complexes and the morphology of the membrane required for the fusion. In myoblasts, associates with CD81 and PTGFRN and inhibits myotube fusion during muscle regeneration. In macrophages, associates with CD9 and beta-1 and beta-2 integrins, and prevents macrophage fusion into multinucleated giant cells specialized in ingesting complement-opsonized large particles. Also prevents the fusion between mononuclear cell progenitors into osteoclasts in charge of bone resorption. Acts as a receptor for PSG17. Involved in platelet activation and aggregation. Regulates paranodal junction formation. Involved in cell adhesion, cell motility and tumor metastasis. Also regulates integrin-dependent migration of macrophages, particularly relevant for inflammatory response in the lung.

In the nervous system, could hydrolyze ATP and other nucleotides to regulate purinergic neurotransmission. Could also be implicated in the prevention of platelet aggregation by hydrolyzing platelet-activating ADP to AMP. Hydrolyzes ATP and ADP equally well.

In the nervous system, could hydrolyze ATP and other nucleotides to regulate purinergic neurotransmission. Could also be implicated in the prevention of platelet aggregation by hydrolyzing platelet-activating ADP to AMP. Hydrolyzes ATP and ADP equally well.

p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.

Hepatocellular carcinoma (HCC) is a major contributor to cancer-related deaths due to its often late stage diagnosis, and dermcidin (DCD) may have the potential to be used as a serum biomarker for HCC for more timely diagnoses. Human dermcidin (DCD) is an antimicrobial peptide secreted constitutively by sweat glands. And the role of DCD in ischemic heart disease has drawn increasing attention in particular its relationship with insulin secretion and glycemic control, nitric oxide (NO) synthesis and hypertension, platelet aggregation and acute myocardial infarction (AMI).

PDE1C belongs to the cyclic nucleotide phosphodiesterase family, PDE1 subfamily. Phosphodiesterases (PDEs) are a family of related phosphohydrolyases that selectively catalyze the hydrolysis of 3' cyclic phosphate bonds in adenosine and or guanine 3',5' cyclic monophosphate (cAMP and or cGMP). They regulate the cellular levels, localization and duration of action of these second messengers by controlling the rate of their degradation. PDEs are expressed ubiquitously, with each subtype having a specific tissue distribution. These enzymes are involved in many signal transduction pathways and their functions include vascular smooth muscle proliferation and contraction, cardiac contractility, platelet aggregation, hormone secretion, immune cell activation, and they are involved in learning and memory. PDE1C has a high affinity for both cAMP and cGMP. It is expressed in several tissues, including brain and heart. As a cyclic nucleotide phosphodiesterase, PDE1C has a dual-specificity for the second messengers cAMP and cGMP.

cGMP-dependent 3',5'-cyclic phosphodiesterase, also known as cyclic GMP-stimulated phosphodiesterase and PDE2A, is a peripheral membrane protein that belongs to the cyclic nucleotide phosphodiesterase family and PDE2 subfamily. Phosphodiesterases (PDEs) comprise a family of enzymes that regulate the levels of cyclic nucleotides, key second messengers that mediate a diverse array of functions. Phosphodiesterases (PDEs) modulate signaling by cyclic nucleotides in diverse processes such as cardiac contractility, platelet aggregation, lipolysis, glycogenolysis, and smooth muscle contraction. PDE2A is an evolutionarily conserved cGMP-stimulated cAMP and cGMP PDE. PDE2A contains two GAF domains. PDE2A is expressed in brain and to a lesser extent in heart, placenta, lung, skeletal muscle, kidney and pancreas. PDE2A is a cyclic nucleotide phosphodiesterase with a dual-specificity for the second messengers cAMP and cGMP, which are key regulators of many important physiological processes. PDE2A is involved in the regulation of blood pressure and fluid homeostasis by the atrial natriuretic peptide (ANP), making PDE2-type enzymes important targets for drug discovery.

Podoplanin belongs to the podoplanin family, also known as Glycoprotein 38. Podoplanin is synthesized as a 172 amino acid (aa) precursor with a 22 aa signal sequence, a 119 aa extracellular domain (ECD), a 21 aa transmembrane region, and a short, 10 aa cytoplasmic tail. Detected at high levels in lung and brain, at lower levels in kidney, stomach, liver, spleen and esophagus, and not detected in skin and small intestine. Expressed in epithelial cells of choroid plexus, ependyma, glomerulus and alveolus, in mesothelial cells and in endothelia of lymphatic vessels. Also expressed in stromal cells of peripheral lymphoid tissue and thymic epithelial cells. Detected in carcinoma cell lines and cultured fibroblasts. Expressed at higher levels in colon carcinomas than in normal colon tissue. It can interacts with CLEC1B; the interaction is independent of CLEC1B glycosylation and activates CLEC1B. It may be involved in cell migration and or actin cytoskeleton organization. When expressed in keratinocytes, induces changes in cell morphology with transfected cells showing an elongated shape, numerous membrane protrusions, major reorganization of the actin cytoskeleton, increased motility and decreased cell adhesion. Required for normal lung cell proliferation and alveolus formation at birth. Ligand for CLEC1B, a platelet receptor. Induces platelet aggregation. Does not have any effect on folic acid or amino acid transport. Does not function as a water channel or as a regulator of aquaporin-type water channels.

Annexin A1 is the first characterized member of the annexin family of proteins and is able to bind to cellular membranes in a calcium-dependent manner, promoting membrane fusion and endocytosis. Annexin A1 has anti-inflammatory properties and inhibits phospholipase A2 activity. Annexin A1 also has roles in many diverse cellular functions, such as membrane aggregation, inflammation, phagocytosis, proliferation, apoptosis, and tumorigenesis and cancer development. ANXA1 is strongly expressed on the cell membrane and occasionally in the cytoplasm of tumor cells in 97% of samples from patients with hairy cell leukemia.

Protein Disulfide-Isomerase A6 (PDIA6) is a 48.5kDa protein that belongs to the protein disulfide isomerase family (PDI). PDIA6 is an enzyme in the endoplasmic reticulum in eukaryotes which catalyzes the formation and breakage of disulfide bonds between cysteine residues within proteins as they fold. The PDIA6 expressed in platelets, its functions as a chaperone that inhibits aggregation of misfolded proteins. PDIA6 is part a large chaperone multiprotein complex comprising DNAJB11, HSP90B1, HSPA5, HYOU, PDIA2, PDIA4, PDIA6, PPIB, SDF2L1, UGT1A1. PDIA6 also plays a role in platelet aggregation and activation by agonists such as convulxin, collagen and thrombin.

Tyrosine-protein kinase Mer (MERTK) is a single-pass type I membrane protein which belongs to the MER AXL TYRO3 receptor kinase family. MERTK include two fibronectin type-III domains, two Ig-like C2-type domains, and one tyrosine kinase domain. It can’t be expressed in normal B- and T-lymphocytes, but it is usually expressed in numerous neoplastic B- and T-cell lines. MERTK could regulate many physiological processes, such as cell survival, migration, differentiation. It was demonstrated that the MERTK plays critical role in the engulfment and efficient clearance of apoptotic cells, platelet aggregation, and cytoskeleton reorganization. Not only these, it also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response by activating STAT1, which selectively induces production of suppressors of cytokine signaling SOCS1 and SOCS3. In addition, MERTK could regulate rod outer segments fragments phagocytosis in the retinal pigment epithelium (RPE)， deficiency in MERTK are the cause of retinitis pigmentosa.

Intrinsically disordered protein acting as a chaperone. Prevents heat-induced aggregation and or inactivation of various substrates. Binds to acidic phospholipid vesicles without affecting membrane fluidity. Dehydrin ERD14 Protein, Arabidopsis thaliana, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 28.1 kDa and the accession number is P42763.

Heat Shock Protein β-11 (HSPB11) is a stress-responsive protein that is required to deal with proteotoxic stresses. HSPB11 is composed of an IFT complex B composed of IFT88, IFT57, TRAF3IP1, IFT52, IFT27, HSPB11 and IFT20 and is detected in placenta. HSPB11 has beeb shown to form oligomeric complexes and prevent the aggregation of in vitro denaturated aldolase and glyceraldehyde-3-phosphate dehydrogenase in accordance with the chaperone model of HSPB1 and HSPB5. HSPB11 overexpression protected against etoposide-induced cell death that correlated with a decreased release of mitochondrial Cytochrome C into the cytosol. Inhibition of HSP90 function completely abrogated the protective effect of HSPB11. This data suggests that at least in the case of HSPB11, interaction with other chaperone machines besides HSPA1A may contribute to functional specificity and cellular functioning.

Elicits platelet aggregation by the binding to the C-type lectin domain family 1 member B (CLEC1B CLEC2). Binding leads to tyrosine phosphorylation in the cytoplasmic tail of CLEC1B, which promotes the binding of spleen tyrosine kinase (Syk), subsequent activation of PLC-gamma-2, and platelet activation and aggregation. Binding to GPIbalpha (GP1BA) and alpha-2 beta-1 (ITGA2 ITGB1) may also induce aggregation, but this is controversial. Snaclec rhodocytin subunit alpha Protein, Calloselasma rhodostoma, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 17.8 kDa and the accession number is Q9I841.

Elicits platelet aggregation by the binding to the C-type lectin domain family 1 member B (CLEC1B CLEC2). Binding leads to tyrosine phosphorylation in the cytoplasmic tail of CLEC1B, which promotes the binding of spleen tyrosine kinase (Syk), subsequent activation of PLCgamma2, and platelet activation and aggregation. Binding to GPIbalpha (GP1BA) and alpha2 beta-1 (ITGA2 ITGB1) may also induce aggregation, but this is controversial. Snaclec rhodocytin subunit beta Protein, Calloselasma rhodostoma, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 21.8 kDa and the accession number is Q9I840.