Cadherin 6/CDH6 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 68 kDa and the accession number is P55285-1.

NOX4 Protein, Human, Recombinant (E. coli, His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 28.8 kDa and the accession number is Q9NPH5.

May play a role in the regulation of extra-urea cycle arginine metabolism and also in down-regulation of nitric oxide synthesis. Extrahepatic arginase functions to regulate L-arginine bioavailability to nitric oxid synthase (NOS). Arginine metabolism is a critical regulator of innate and adaptive immune responses. Seems to be involved in negative regulation of the survival capacity of activated CD4(+) and CD8(+) T cells. May suppress inflammation-related signaling in asthmatic airway epithelium. May contribute to the immune evasion of H.pylori by restricting M1 macrophage activation and polyamine metabolism. May play a role in promoting prenatal immune suppression. Regulates RPS6KB1 signaling, which promotes endothelial cell senescence and inflammation and implicates NOS3/eNOS dysfunction. Can inhibit endothelial autophagy independently of its enzymatic activity implicating mTORC2 signaling. Involved in vascular smooth muscle cell senescence and apoptosis independently of its enzymatic activity.

Cadherin 6/CDH6 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 68.7 kDa and the accession number is P97326.

NOX4 Protein, Human, Recombinant (Cell-Free, His) is expressed in E. coli expression system with N-10xHis tag. The predicted molecular weight is 69.8?kDa and the accession number is Q9NPH5.

May be involved in processing of pneumocyte surfactant precursors. Napsin-A/NAPSA Protein, Mouse, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 40.5 kDa and the accession number is O09043.

Polycystin-1 Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 69.3 kDa and the accession number is P98161.

Cadherin-6 (CDH6) is a type-II classic cadherin cell-cell adhesion molecules, which are expressed in graded or areal patterns, as well as layer-specific patterns, in the cortical plate. Human Cadherin-6 is synthesized as a 790 aa type I transmembrane glycoprotein that contains a 18 aa signal peptide, a 35 aa propeptide, a 562 aa extracellular region, a 21 aa transmembrane segment, and a 154 aa cytoplasmic domain. There are five cadherin domains of approximately 110 aa each in the extracellular region. Cadherin-6 has high expression in kidney, brain, and cerebellum, and may contribute to the formation of the segmental structure of the early brain, as well as the development of renal proximal tubules. Weak expression is also detected in lung, pancreas, gastric mucosa and cytotrophoblasts. As a classic cadherin, Cadherin-6 will form homodimers and promote intercellular adhesion with itself and, possibly, Cadherin-9 and -14.

TIM-1/KIM-1/HAVCR belongs to the immunoglobulin superfamily that cosisits 305 amino acid (aa). It is expressed by stimulated T-cells. TIM-1/KIM-1/HAVCR may play a role in T-helper cell development and the regulation of asthma and allergic diseases. Receptor for TIMD4. And may have a role in kidney injury and repair. Belongs to the T-cell and airway phenotype regulator (Tapr) locus, a single chromosomal region that confers reduced T-helper type 2 responsiveness and protects against airway hyperactivity (AHR), the hallmark of human asthma.

Aquaporin-1/AQP1 Protein, Human, Recombinant (His & SUMO) is expressed in E. coli.

Collectin-11 is a secreted protein that belongs to the COLEC10/COLEC11 family. Collectin-11 contains one C-type lectin domain and one collagen-like domain. Collectins play important roles in the innate immune system by binding to carbohydrate antigens on microorganisms, facilitating their recognition and removal. Collectin-11 binds to various sugars including fucose and mannose, but does not bind to glucose, N-acetylglucosamine and N-acetylgalactosamine. It has a higher affinity for fucose compared to mannose. Collectin-11 binds lipopolysaccharides (LPS). It also involved in fundamental development serving as a guidance cue for neural crest cell migration. Defects in Collectin-11 are the cause of 3MC syndrome type 2 (3MC2).

Alkaline Phosphatase/ALPL Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 55 kDa and the accession number is B7XGA6.

Alkaline Phosphatase/ALPL Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 55 kDa and the accession number is A0A024RAB4.

Kallikrein-1 (KLK1) is a member of human tissue Kallikrein family. Human KLK1 precursor contains a singal peptide (residues 1 to 18), a short pro peptide (residues 19 to 24) and a mature chain (residues 25 to 262). The function of KLK1 is to cleave Kininogen in order to release the vasoactive Kinin peptide (Lysyl-Bradykinin or Bradykinin). The Kinin peptide controls blood pressure reduction, vasodilation, smooth muscle relaxation and contraction, pain induction and inflammation. KLK1 also plays a role in angiogensis and tumorigenesis.

Arginase-2 (ARG2) is a member of the arginase family. Arginase is a manganese-containing enzyme which catalyzes the hydrolysis of arginine to ornithine and urea. ARG2 is highly expressed in kidney and prostate, not founded in the liver, heart and pancreas. ARG2 has been implicated in the regulation of the arginine/ornithine concentrations in the cell. ARG2 may take part in the regulation of extra-urea cycle arginine metabolism and in down-regulation of nitric oxide synthesis. The extrahepatic arginase functions to regulate L-arginine bioavailability to NO synthase.

Cadherin 6/CDH6 Protein, Rat, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 67.9 kDa and the accession number is A6KJN4.

Alkaline Phosphatase/ALPL Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 80.3 kDa and the accession number is B7XGA6.

Cadherin 6/CDH6 Protein, Cynomolgus, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 67.5 kDa and the accession number is XP_005556691.1.

Dickkopf-related protein 1 (DKK-1), a ligand for the WNT coreceptors low-density lipoprotein receptor-related proteins 5 and 6 (LRP-5 and LRP-6) and an inhibitor of WNT/β-catenin signaling, effectively inhibits pericyte activation, detachment, and transition to myofibroblasts in vivo in response to kidney injury, resulting in attenuated fibrogenesis, capillary rarefaction, and inflammation.LRP-6 interacts closely with PDGF receptor β and TGF-β receptor 1 at the cell membrane, suggesting that it may have roles in pathways other than WNT/β-catenin.

Serpin E2 is a member of the Serpin superfamily. It is differentially expressed during neuronal differentiation and is able to transform human embryonic kidney cells into neuronlike cells. Its over-expression in mice leads to progressive neuronal and motor dysfunction in these animals. It is also over-expressed in the majority of pancreatic carcinoma as well as gastric and colorectal cancer samples whereas it is weakly expressed in all normal pancreas and chronic pancreatitis tissue samples. Serpin E2 is a potent inhibitor of thrombin, trypsin, urokinase, plasmin and plasminogen activators. It plays an important role in controlling male fertility because its knockout male mice show a marked impairment in fertility from the onset of sexual maturity and its abnormal expression is found in the semen of men with seminal dysfunction.

Heat-Responsive Protein 12 (HRSP12) is an endoribonuclease that belongs to the Rut family. HRSP12 is found mainly in the human adult kidney and liver and is responsible for inhibiting protein translation by cleaving mRNA. HRSP12 only cleaves phosphodiester bonds in single-stranded RNA and inhibits cell-free protein synthesis. The levels of both mRNA and protein are markedly reduced in heptatocellular tumors and in human hepatoma cell lines compared with normal liver tissues. Moreover the levels of HRSP12 are different depending on the grade of the tumor. This had led to the suggestion that HRSP12 may be an important biomarker for heptatic carcinoma.

Lipocalin-2, also known as Neutrophil Gelatinase-Associated Lipocalin (NGAL), is a secretory protein of the lipocalin superfamily. Lipocalin-2 contains a signal peptide that enables it to be secreted and form complexes with matrix metalloproteinase-9 (MMP-9) through disulfide bonds. Similar to other lipocalin family members, Lipocalin-2 is involved in diverse cellular processes, including the transport of small hydrophobic molecules, protection of MMP-9 from proteolytic degradation, and cell signaling. Furthermore, Lipocalin-2 can tightly bind to bacterial siderophore through a cell surface receptor, possibly serving as a potent bacteriostatic agent by sequestering iron, regulating innate immunity and protecting kidney epithelial cells from ischemia–reperfusion injury. This protein is mainly expressed in neutrophils and in lower levels in the kidney, prostate, and epithelia of the respiratory and alimentary tracts.Recent evidence also suggests its role as a biomarker for renal injury and inflammation.

Angiopoietin-like 2 (ANGPTL2) is a proinflammatory protein belonging to the angiopoietin-like family. ANGPTL2 is secreted and detected in the systemic circulation. Different observational clinical studies reported that circulating levels of ANGPTL2 increase significantly in various chronic inflammatory diseases and showed associations between ANGPTL2 levels and diagnosis and/or prognosis of cardiovascular diseases, diabetes, chronic kidney disease, and various types of cancers. ANGPTL2 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 30.1 kDa and the accession number is Q9UKU9-1.

Kidney injury molecule 1 (KIM-1, also known as TIM-1) is markedly upregulated in the proximal tubule after injury and is maladaptive when chronically expressed. KIM-1-mediated epithelial cell phagocytosis of apoptotic cells protects the kidney after acute injury by downregulating innate immunity and inflammation. TIM-1/KIM-1/HAVCR1 Protein, Cynomolgus, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 35.25 kDa and the accession number is A0A2K5WXJ6.

Mouse Cxcl12 is a secreted and highly conserved protein which belongs to the intercrine alpha (chemokine CxC) family.CXCL12 is widely expressed in various organs including brain, kidney, skeletal muscle, heart, liver, and lymphoid organs. Cxcl12 activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis. It also binds to atypical chemokine receptor ACKR3 which activates the beta-arrestin pathway and acts as a scavenger receptor for SDF-1. Cxcl12 has several critical functions during embryonic development such as B-cell lymphopoiesis, myelopoiesis in bone marrow and heart ventricular septum formation. Cxcl12 plays an important role in acting as a positive regulator of monocyte migration and a negative regulator of monocyte adhesion via the LYN kinase. It stimulates migration of monocytes and T-lymphocytes through its receptors, CXCR4 and ACKR3, and decreases monocyte adherence to surfaces coated with ICAM-1, a ligand for beta-2 integrins. SDF1A/CXCR4 signaling axis inhibits beta-2 integrin LFA-1 mediated adhesion of monocytes to ICAM-1 through LYN kinase. It also plays a protective role after myocardial infarction, induces down-regulation and internalization of ACKR3 expressed in various cells and stimulates the proliferation of bone marrow-derived b progenitor cells in the presence of IL-7 as well as growth of the stromal cell-dependent B-cell clone DW34 cells.

Butyrophilin 2A1 (BTN2A1) is an approximately widely expressed and variably glycosylated type I transmembrane glycoprotein. Mature human Butyrophilin 2A1 consisits of a 220 amino acid (aa) extracellular domain with two immunoglobulin-like domains, a 21 aa transmembrane segment, and a 258 aa cytoplasmic domain. Alternative splicing generates additional isoforms of human Butyrophilin 2A1 that lack the first Ig like domain or transmembrane segment as well as isoforms with substitutions and deletions in the cytoplasmic region. BTN2A1 is widely expressed including on colonic epithelial cells, on immune cells, and in milk fat globules. It binds to the C-type lectin DCSIGN on monocytederived dendritic cells, and this interaction can be blocked by soluble gp130 from HIV. The polymorphism of BTN2A1 has been associated with metabolic syndrome, type II diabetes mellitus, chronic kidney disease, and hypertension.

TINAGL1 is a secreted protein and contains one SMB (somatomedin-B) domain. TINAGL1 is expressed in aorta, lymph nodes, heart, bone marrow, placenta, lung, kidney, skeletal muscle, pancreas, thyroid, adrenal gland and so on. TINAGL1 may be implicated in the adrenocortical zonation and in mechanisms for repressing the CYP11B1 gene expression in adrenocortical cells.

Connective tissue growth factor (CTGF) is a member of the CCN matricellular protein family, consisting of four domains, that regulates the signaling of other growth factors and promotes kidney fibrosis.CTGF can simultaneously interact with several factors with its four domains. The microenvironment differs depending on the types of cells and tissues and differentiation stages of these cells. CTGF/CCN2 Protein, Rhesus macaque, Recombinant (His) is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 36.52 kDa and the accession number is H9FQD5.

Mouse Ephrin-B1 is a single-pass type I membrane protein which belongs to the ephrin family. It contains an ephrin RBD (ephrin receptor-binding) domain, and expressed in heart, placenta, lung, liver, skeletal muscle, kidney and pancreas. Ephrin-B1 is cell surface transmembrane ligand for Eph receptors, a family of receptor tyrosine kinases which are crucial for migration, repulsion and adhesion during neuronal, vascular and epithelial development. It binds promiscuously Eph receptors residing on adjacent cells, leading to contact-dependent bidirectional signaling into neighboring cells. It may play a role in cell adhesion and function in the development or maintenance of the nervous system.

Cardiotrophin-1, also known as CT-1 and CTF1, is a member of the IL-6 superfamily. It is a sreted cytokine that is expressed in heart, skeletal muscle, prostate and ovary, and to lower levels in lung, kidney, pancreas, thymus, testis and small intestine. The protein exerts its cellular effects by interacting with the glycoprotein 130 (gp130)/leukemia inhibitory factor receptor beta (LIFR) heterodimer. In addition, CT-1 activates phosphatidylinositol 3-kinase (PI-3 kinase) in cardiac myocytes and enhances transcription factor NF-κB DNA -binding activities.

Annexin A13 (ANXA13) belongs to the annexin family which plays a role in phospholipase inhibition, cytoskeletal interactions, intracellular signal transduction pathways and regulation of cellular growth. ANXA13 contains four annexin repeats and a pair of annexin repeats may form one binding site for calcium and phospholipid. ANXA13 is highly expressed in intestinal and kidney epithelial cells. The specific function of ANXA13 has not yet been determined; however it is associated with the plasma membrane of undifferentiated, proliferating crypt epithelial cells as well as differentiated villus enterocytes.

Chloride intracellular channel protein 4, also known as Intracellular chloride ion channel protein p64H1 and CLIC4, is a member of the chloride channel CLIC family. It contains oneGST C-terminal domain. CLIC4 is a member of a family of intracellular chloride channels. It is regulated by p53, c-Myc, and tumor necrosis factor-alpha. CLIC4 is detected in epithelial cells from colon, esophagus and kidney (at protein level). CLIC4 has alternate cellular functions like a potential role in angiogenesis or in maintaining apical-basolateral membrane polarity during mitosis and cytokinesis. CLIC4 could promote endothelial cell proliferation and regulate endothelial morphogenesis (tubulogenesis). Expression of CLIC4 is prominent in heart, kidney, placenta and skeletal muscle. Overexpression of CLIC4 in cancer cells inhibits tumor growth. Conversely, overexpression of CLIC4 in tumor stromal cells stimulates tumor growth. Thus, CLIC4 participates in normal and pathological processes and may serve as a useful target for therapies in disturbances of homeostasis and neoplastic transformation. Loss of CLIC4 in tumor cells and gain in tumor stroma is common to many human cancers and marks malignant progression. Up-regulation of CLIC4 in tumor stroma is coincident with myofibroblast conversion, generally a poor prognostic indicator. Reactivation and restoration of CLIC4 in tumor cells or the converse in tumor stromal cells could provide a novel approach to inhibit tumor growth.

DCX (doublecortin, N-GST chimera)contains 2 doublecortin domains and belongs to the doublecortin family. It is highly expressed in neuronal cells of fetal brain, but not expressed in other fetal tissues. In the adult, it is highly expressed in the brain frontal lobe, but very low expression in other regions of brain, and not detected in heart, placenta, lung, liver, skeletal muscles, kidney and pancreas. DCX is a microtubule-associated protein required for initial steps of neuronal dispersion and cortex lamination during cerebral cortex development. It may act by competing with the putative neuronal protein kinase DCAMKL1 in binding to a target protein. DCX may in that way participate in a signaling pathway that is crucial for neuronal interaction before and during migration, possibly as part of a calcium ion-dependent signal transduction pathway. It may be part with LIS-1 of a overlapping, but distinct, signaling pathways that promote neuronal migration. Defects in DCX are the cause of lissencephaly X-linked type 1 and subcortical band heterotopia X-linked.

Actopaxin, also known as alpha-parvin, belongs to the parvin family. It is widely expressed, with highest levels in heart, skeletal muscle, kidney and liver. Actopaxin contains 2 CH (calponin-homology) domains and probably plays a role in the regulation of cell adhesion and cytoskeleton organization. It interacts with integrin-linked protein kinase and probably with actin and the LD1 and LD4 motifs of PXN. Actopaxin binds directly to both F-actin and paxillin LD1 and LD4 motifs. Actopaxin also exhibits robust focal adhesion localization in several cultured cell types but is not found along the length of the associated actin-rich stress fibers. It is absent from actin-rich cell-cell adherens junctions.

Caspase 7, also known as caspase-7 and MCH3, belongs to the cysteine-aspartic acid protease (caspase) family. Caspases play a role in the signal transduction pathways of apoptosis, necrosis and inflammation. There are two major classes of caspases: initiators and effectors. The initiator isoforms (caspases-1,-4,-5,-8,-9,-10,-11,-12) are activated by, and interact with, upstream adaptor molecules through protein-protein interaction domains known as CARD and DED. Effector caspases (-3,-6,-7) are responsible for cleaving downstream substrates and are sometimes referred to as the executioner caspases. Caspase 7 exists in lung, skeletal muscle, liver, kidney, spleen, heart, and moderately in testis. Caspase 7 cannot be detected in the brain. Caspase 7 functions in the activation cascade of caspases responsible for apoptosis execution. It cleaves and activates sterol regulatory element binding proteins (SREBPs). It proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a '216-Asp- -Gly-217' bond. Overexpression promotes programmed cell death.

C1D nuclear receptor corepressor belongs to the C1D family. It is a DNA binding and apoptosis-inducing protein.C1D nuclear receptor corepressorinteracts with TSNAX and DNA-PKcs. It acts as a corepressor for the thyroid hormone receptor. It is thought that C1D nuclear receptor corepressor regulates TRAX/Translin complex formation. It is expressed in kidney, heart, brain, spleen, lung, testis, liver and small intestine. It plays a role in the recruitment of the RNA exosome complex to pre-rRNA to mediate the 3'-5' end processing of the 5.8S rRNA; this function may include MPHOSPH6. It potentiates transcriptional repression by NR1D1 and THRB. C1D nuclear receptor corepressorcan activate PRKDC not only in the presence of linear DNA but also in the presence of supercoiled DNA. It also can induce apoptosis in a p53/TP53 dependent manner.

acidic leucine-rich nuclear phosphoprotein 32 family member A, also known as acidic nuclear phosphoprotein pp32, Leucine-rich acidic nuclear protein, Mapmodulin, Potent heat-stable protein phosphatase 2A inhibitor I1PP2A, Putative HLA-DR-associated protein I, PHAPI and ANP32A, is a nucleus, cytoplasm and endoplasmic reticulum. ANP32A / LANP is expressed in all tissues tested. It is highly expressed in kidney and skeletal muscle, moderate levels of expression is in brain, placenta and pancreas. ANP32A / LANP is weakly expressed in lung. It is found in all regions of the brain examined (amygdala, caudate nucleus, corpus callosum, hippocampus and thalamus), with highest levels in amygdala. ANP32A / LANP is a component of the SET complex, which also contains SET, APEX1, HMGB2 and NME1. It directly interacts with SET. ANP32A / LANP also interacts with ATXN1/SCA1. ANP32A / LANP is implicated in a number of cellular processes, including proliferation, differentiation, caspase-dependent and caspase-independent apoptosis, suppression of transformation (tumor suppressor), inhibition of protein phosphatase 2A, regulation of mRNA trafficking and stability in association with ELAVL1, and inhibition of acetyltransferases as part of the INHAT (inhibitor of histone acetyltransferases) complex. ANP32A / LANP plays a role in E4F1-mediated transcriptional repression.

Beta-defensin 3 is a member of the defensin family. Defensin family is comprised by microbicidal and cytotoxic peptides made by neutrophils. Members of the beta-defensin 3 family are highly similar in protein sequence. Beta-defensin 3 shows antimicrobial activity against Gram-positive bacteria S.aureus and S.pyogenes, Gram-negative bacteria P.aeruginosa and E.coli and the yeast C.albicans. Beta-defensin 3 is abundantly expressed in skin and tonsils, and to a lesser extent in trachea, uterus, kidney, thymus, adenoid, pharynx and tongue. It is also expressed in salivary gland, bone marrow, colon, stomach, polyp and larynx. However, in small intestine, it cannot be detected. Defensin has broad spectrum antimicrobial activity and may play an important role in innate epithelial defense. Beta-defensin 3 kills multiresistant S.aureus and vancomycin-resistent E.faecium. It has no significant hemolytic activity.

Leucine-rich repeat transmembrane protein FLRT3, also known as Fibronectin-like domain-containing leucine-rich transmembrane protein 3, and FLRT3, is a single-pass type I membrane protein which belongs to the fibronectin leucine rich transmembrane protein (FLRT) family. FLRT3 contains one fibronectin type-III domain and ten LRR (leucine-rich) repeats and is expressed in kidney, brain, pancreas, skeletal muscle, lung, liver, placenta, and heart. It has a provocative expression pattern during somite development being expressed in regions of the somite where muscle precursor cells migrate from the dermomyotome and move into the myotome, and later in myotomal precursors destined to migrate towards their final destination. FLRT1, FLRT2 and FLRT3 are members of the FLRT family. The FLRT family of leucine-rich repeat (LRR) proteins is implicated in fibroblast growth factor (FGF) signalling, early embryonic development and neurite outgrowth. FLRT3 shares 55% amino acid sequence identity with FLRT1 and 44% identity with FLRT2. Two alternatively spliced transcript variants encoding the same protein have been described. The expression of FLRT3 is controlled by fibroblast growth factors (FGFs). FLRT3 has been implicated in neurite outgrowth after nerve damage, as a positive regulator of FGF signalling and in homotypic cell adhesion. FLRT3 may have a crucial role in regulating cellular adhesion between the epithelial apical ridge and the underlying mesenchyme and in establishing the dorso-ventral position of the ridge.

IDO2 belongs to the indoleamine 2,3-dioxygenase family. Indoleamine 2,3-dioxgyenase (IDO), is a cytosolic haem protein which, together with the hepatic enzyme tryptophan 2,3-dioxygenase, catalyzes the conversion of tryptophan and other indole derivatives to kynurenines. In addition to classic IDO (IDO1), a new variant, IDO2, has recently been described. IDO2 is expressed in the liver, small intestine, spleen, placenta, thymus, lung, brain, kidney, and colon. IDO is widely distributed in human tissues, its physiological role is not fully understood but is of great interest. IDO can be up-regulated via cytokines such as interferon-gamma, and can thereby modulate the levels of tryptophan, which is vital for cell growth. In humans and mice, the IDO1 and IDO2 genes are present tandemly in a tail-to-head arrangement on chromosome 8. In lower vertebrates such as zebrafish and toads, only a single IDO gene may be present that may be more IDO2-like in structure. This closer relationship to IDO2 suggests that IDO2 may be the ancestor of the better characterized IDO1 gene and that IDO1 might have been generated by gene duplication of IDO2 before the origin of tetrapods in mammalian evolutionary history. IDO2 catalyzes the first and rate-limiting step in the kynurenine pathway of tryptophan catabolism.

Suppressor of cytokine signaling 3, also known as SOCS-3, Cytokine-inducible SH2 protein 3, CIS-3, STAT-induced STAT inhibitor 3, SOCS3 and CIS3, is a protein which is widely expressed with high expression in heart, placenta, skeletal muscle, peripheral blood leukocytes, fetal and adult lung, and fetal liver and kidney. SOCS3 / CIS3 contains one SH2 domain and one SOCS box domain. SOCS family proteins form part of a classical negative feedback system that regulates cytokine signal transduction. SOCS3 / CIS3 is involved in negative regulation of cytokines that signal through the JAK / STAT pathway. SOCS3 / CIS3 inhibits cytokine signal transduction by binding to tyrosine kinase receptors including gp13, LIF, erythropoietin, insulin, IL12, GCSF and leptin receptors. Binding to JAK2 inhibits its kinase activity. SOCS3 / CIS3 suppresses fetal liver erythropoiesis. It regulates onset and maintenance of allergic responses mediated by T-helper type 2 cells. SOCS3 / CIS3 regulates IL-6 signaling. SOCS3 / CIS3 interacts with multiple activated proteins of the tyrosine kinase signaling pathway including IGF1 receptor, insulin receptor and JAK2. SOCS3 / CIS3 could be used as a possible therapeutic agent for treating rheumatoid arthritis.

Protein arginine N-methyltransferase 6, also known as Histone-arginine N-methyltransferase PRMT6, PRMT6, and HRMT1L6, is a member of the protein arginine N-methyltransferase family and PRMT6 subfamily. PRMT6 is highly expressed in kidney and testes. PRMT6 is known to catalyze the generation of asymmetric dimethylarginine in polypeptides. It has been implicated in human immunodeficiency virus pathogenesis, DNA repair, and transcriptional regulation. PRMT6 is known to methylate histone H3 Arg-2 (H3R2), and this negatively regulates the lysine methylation of H3K4 resulting in gene repression. PRMT6 plays a key role in coupling process by functioning as a transcriptional coactivator that can regulate alternative splicing. PRMT6 coactivates the progesterone, glucocorticoid and oestrogen receptors in luciferase reporter assays in a hormone-dependent manner. Small interfering RNA (siRNA) oligonucleotide duplex knockdown of PRMT6 disrupts oestrogen-stimulated transcription of endogenous GREB1 and progesterone receptor in MCF-7 breast cancer cells. Neutralizing the activity of PRMT6 could inhibit tumor progression and may be of cancer therapeutic significance.

The three fibronectin leucine-rich repeat transmembrane (FLRT) proteins contain 10 leucine-rich repeats (LRR), a type III fibronectin (FN) domain, followed by the transmembrane region, and a short cytoplasmic tail. FLRT1 is expressed in kidney and brain, which is a target for tyrosine phosphorylation mediated by FGFR1 and implicates a non-receptor Src family kinase (SFK). All FLRTs can interact with FGFR1 and FLRTs can be induced by the activation of FGF signalling by FGF-2. The phosphorylation state of FLRT1, which is itself FGFR1 dependent, may play a critical role in the potentiation of FGFR1 signalling and may also depend on a SFK-dependent phosphorylation mechanism acting via the FGFR. This is consistent with an 'in vivo' role for FLRT1 regulation of FGF signalling via SFKs. Furthermore, the phosphorylation-dependent futile cycle mechanism controlling FGFR1 signalling is concurrently crucial for regulation of FLRT1-mediated neurite outgrowth. FLRT1, FLRT2 and FLRT3 are members of the fibronectin leucine rich transmembrane protein (FLRT) family. They may function in cell adhesion and/or receptor signalling. Their protein structures resemble small leucine-rich proteoglycans found in the extracellular matrix. FLRT3 shares 55% amino acid sequence identity with FLRT1.

Harmonin, also known as Antigen NY-CO-38 / NY-CO-37, Autoimmune enteropathy-related antigen AIE-75, Protein PDZ-73, Renal carcinoma antigen NY-REN-3, Usher syndrome type-1C protein and USH1C, is a protein that is expressed in small intestine, colon, kidney, eye and weakly in pancreas. USH1C is expressed also in vestibule of the inner ear. USH1C contains 3 PDZ (DHR) domains. USH1C may be involved in protein-protein interaction. Defects in USH1C are the cause of Usher syndrome type 1C (USH1C), also known as Usher syndrome type I Acadian variety. USH is a genetically heterogeneous condition characterized by the association of retinitis pigmentosa and sensorineural deafness. Age at onset and differences in auditory and vestibular function distinguish Usher syndrome type 1 (USH1), Usher syndrome type 2 (USH2) and Usher syndrome type 3 (USH3). Defects in USH1C are also the cause of deafness autosomal recessive type 18 (DFNB18) which is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information.

Endothelin-converting enzyme 1, also known as ECE-1, is a single-pass type II membrane protein which belongs to thepeptidase M13 family. ECE-1 converts big endothelin-1 to endothelin-1. ECE-1 is a membrane metalloprotease that generates endothelin from its direct precursor big endothelin. Four isoforms of ECE-1 are produced from a single gene through the use of alternate promoters. These isoforms share the same extracellular catalytic domain and contain unique cytosolic tails, which results in their specific subcellular targeting.All isoforms of ECE-1 are expressed in umbilical vein endothelial cells, polynuclear neutrophils, fibroblasts, atrium cardiomyocytes and ventricles. Isoforms A, B and C of ECE-1 are also expressed in placenta, lung, heart, adrenal gland and phaeochromocytoma; isoforms A and C of ECE-1 in liver, testis and small intestine; isoform B, C and D of ECE-1 in endothelial cells and umbilical vein smooth muscle cells; isoforms C and D in saphenous vein cells, and isoform C in kidney. Defects in ECE1 are a cause of Hirschsprung disease, cardiac defects and autonomic dysfunction. It is a form of Hirschsprung disease with skip-lesions defects, craniofacial abnormalities and other dysmorphic features, and autonomic dysfunction.

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is a member of the IGF-II mRNA-binding protein (IMP) family. IGF2BP2 is a member of a family of mRNA binding proteins that, collectively, have been shown to bind to several different mRNAs in mammalian cells, including one of the mRNAs encoding insulin-like growth factor-2. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is involved in the stimulation of insulin action. IGF2BP2 / IMP2 is expressed in oocytes, granulosa cells of small and growing follicles, Leydig cells, spermatogonia, and semen (at protein level). It is also expressed in testicular cancer (at protein level). It is expressed weakly in the heart, placenta, skeletal muscle, bone marrow, colon, kidney, salivary glands, testis, and pancreas. IGF2BP2 binds to the 5'-UTR of the insulin-like growth factor 2 (IGF2) mRNAs. This binding is isoform-specific. IGF2BP2 may regulate the translation of target mRNAs.

SULT1A3 belongs to the sulfotransferase 1 family. Sulfotransferase enzymes catalyze the sulfate conjugation of many hormones, neurotransmitters, drugs, and xenobiotic compounds. They are different in their tissue distributions and substrate specificities while their gene structure (number and length of exons) is similar. SULT1A3 gene encodes a phenol sulfotransferase with thermolabile enzyme activity. Four sulfotransferase genes are located on the p arm of chromosome 16; this gene and SULT1A4 arose from a segmental duplication. It is the most centromeric of the four sulfotransferase genes. Exons of this gene overlap with exons of a gene that encodes a protein containing GIY-YIG domains (GIYD1). SULT1A3 is expressed in liver, colon, kidney, lung, brain, spleen, small intestine, placenta and leukocyte. SULT1A3 is a sulfotransferase that utilizes 3'-phospho-5'-adenylyl sulfate (PAPS) as sulfonate donor to catalyze the sulfate conjugation of phenolic monoamines (neurotransmitters such as dopamine, norepinephrine and serotonin) and phenolic and catechol drugs.

Tribbles homolog 3, also known as Neuronal cell death-inducible putative kinase, p65-interacting inhibitor of NF-kappa-B, SINK and TRIB3, is a Nucleus protein that belongs to the protein kinase superfamily and CAMK Ser/Thr protein kinase family and Tribbles subfamily. Highest expression Of TRIB3 is in liver, pancreas, peripheral blood leukocytes and bone marrow. It is also highly expressed in a number of primary lung, colon and breast tumors. TRIB3 is expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney. TRIB3 disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. TRIB3 may bind directly to and mask the 'Thr-38' phosphorylation site in AKT1. It binds to ATF4 and inhibits its transcriptional activation activity. TRIB3 interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. It interacts with MAPK kinases and regulates activation of MAP kinases. It may play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. TRIB3 does not display kinase activity.

Serine / threonine-protein kinase Sgk3, also known as Serum / glucocorticoid-regulated kinase 3, Serum / glucocorticoid-regulated kinase-like and SGK3, is a cytoplasmic vesicle protein that belongs to the protein kinase superfamily and AGC Ser/Thr protein kinase family. SGK3 contains one AGC-kinase C-terminal domain, one protein kinase domain and one PX (phox homology) domain. Two specific sites of SGK3, one in the kinase domain (Thr-32) and the other in the C-terminal regulatory region (Ser-486), is needed to be phosphorylated for its full activation. SGK3 is expressed in most tissues with highest levels in pancreas, kidney liver, heart and brain and lower levels in lung, placenta and skeletal muscle. SGK3 is involved in the activation of potassium channels. It mediates cell IL-3-dependent survival signals. SGK3 participates in the regulation of HERG by increasing HERG protein abundance in the plasma membrane and may thus modify the duration of the cardiac action potential. SGK3 is also a very important and characteristic molecule that plays a critical role in both hair follicle morphogenesis and hair cycling.

Serine / threonine-protein kinase SRPK1, also known as SFRS protein kinase 1, Serine/arginine-rich protein-specific kinase 1, SR-protein-specific kinase 1 and SRPK1, is a cytoplasm and nucleus protein that belongs to the protein kinase superfamily and CMGC Ser/Thr protein kinase family. Isoform 2 of SRPK1 is predominantly expressed in the testis but is also present at lower levels in heart, ovary, small intestine, liver, kidney, pancreas and skeletal muscle. Isoform 1 of SRPK1 is only seen in the testis, at lower levels than isoform 2. SRPK1 hyperphosphorylates RS domain-containing proteins such as SFRS1, SFRS2 and ZRSR2 on serine residues during metaphase but at lower levels during interphase. SRPK1 plays a central role in the regulatory network for splicing, controlling the intranuclear distribution of splicing factors in interphase cells and the reorganization of nuclear speckles during mitosis. SRPK1 locks onto SFRS1 to form a stable complex and processively phosphorylates the RS domain. SRPK1 appears to mediate HBV core protein phosphorylation which is a prerequisite for pregenomic RNA encapsidation into viral capsids.