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IL-17F having an accession number of Q96PD4 is a cytokine that shares sequence similarity with IL17. IL-17F is expressed by activated T cells, and has been shown to stimulate the production of several other cytokines, including IL6, IL8, and CSF2/GM-CSF. IL-17F inhibits the angiogenesis of endothelial cells and induce endothelial cells to produce IL2, TGFB1/TGFB, and monocyte chemoattractant protein-1. IL-17F induces stromal cells to produce proinflammatory and hematopoietic cytokines. Intestinal IL17F gene expression is increased in active CD.
IL-17A & IL-17F alleles influence the susceptibility to and pathophysiological features of ulcerative colitis independently. IL-17F and MIF gene polymorphisms are significantly associated with the development of functional dyspepsia.
The initiation of IL-17F/IL-17R signaling pathway requires the receptor ubiquitination by TRAF6. IL-17F induces expression of IFN-gamma-inducible protein 10 (IP-10) by activating Raf1-mitogen-activated protein kinase 1/2-extracellular-regulated kinase 1/2-p90 ribosomal S6 kinase-cyclic AMP response element-binding protein signaling pathway.

SERPINA1 is secreted and is a serine protease inhibitor which its targets include elastase, plasmin, collagenase, thrombin, leucocytic proteases, trypsin, chymotrypsin, and plasminogen activator. Defects in SERPINA1 gene can cause emphysema or liver disease. Antral SERPINA1 expression is particularly induced by H. pylori infection. lung and prostate cancers have shown a significant increase in SERPINA1 serum levels compared with healthy controls though breast cancers did not show a significant change. SERPINA1 is an endogenous inhibitor of serine proteases and inhibits the catalytic domain of human recombinant matriptase in vitro. Rise in SERPINA1 occurs as an acute phase response to tissue necrosis and inflammation. mutations in SERPINA1 and SLC11A1 genes change the balance between elastase produced by leukocytes during phagocytosis.

SLAMF1 is a member of the immunoglobulin gene superfamily and is involved in T-cell stimulation. The SLAMF1 protein is constitutively expressed on peripheral blood memory T cells, T-cell clones, immature thymocytes, and a fraction of B cells, and is swiftly induced on naive T cells after activation. There are probably 2 modes of SLAM signaling: one in which the inhibitor SH2D1A serves as a negative regulator and another in which protein-tyrosine phosphatase 2C (PTPN11)-dependent signal transduction functions.

BRCA2 And CDKN1A Interacting Protein (BCCIP) is a nuclear protein with multiple interacting domains which remained conserved throughout the evolution. BCCIP is an important cofactor for BRCA2 in tumor suppression, and a modulator of CDK2 kinase activity via p21. BCCIP takes also part in the regulation of BRCA2 and RAD51 nuclear focus formation, doublestrand break-induced homologous recombination, and cell cycle progression.

Truncated BH3 interacting domain death agonist is a truncated form of the pro-apoptotic full-length BID. Truncated BH3 interacting domain death agonist is generated by Caspase-8 cleavage of BID. The truncated form of the protein translocates from the cytosol to mitochondria and transduces apoptotic signals.
BID is a pro-apoptotic Bcl-2 protein having only the BH3 domain. In reaction to apoptotic signaling, BID interacts with another Bcl-2 family of cell death regulators, called Bax, they form a heterodimer resulting to the insertion of Bax into the outer mitochondrial membrane. Bax induces the opening of the mitochondrial voltage-dependent anion channel which lead to the release of cytochrome c and other pro-apoptotic factors from the mitochondria resulting in activation of caspases. BID is a mediator of mitochondrial damage induced by caspase-8 (CASP8). CASP8 cleaves BID, and the COOH-terminal part translocates to mitochondria where it triggers cytochrome c release. The major proteolytic product p15 BID releasea cytochrome c. Isoform 1, Isoform 2 and Isoform 4 induce ice-like proteases and apoptosis while Isoform 3 does not induce apoptosis.

CAB39 protein and STE20-related adaptor-alpha pseudo kinase, form a regulatory complex that is able of stimulating the activity of the LKB1 tumor suppressor protein kinase. CAB39 takes part as a scaffolding component of the STK11/STRAD complex and regulates STK11 activity and cellular localization.

Fibronectin Leucine Rich Transmembrane Protein 3, also known as FLRT3 is a member of the fibronectin leucine rich transmembrane protein (FLRT) family. FLRT3 contains one fibronectin type-III domain as well as 10 LRR (leucine-rich) repeats and is expressed in the kidney, brain, pancreas, skeletal muscle, lung, liver, placenta, and heart. In addition, the members of the FLRT family play a role in cell adhesion as well as receptor signaling. FLRT3 has been implicated in neurite outgrowth after nerve damage, as a positive regulator of FGF signalling and in homotypic cell adhesion. Furthermore, FLRT3 has an essential function in regulating cellular adhesion among the epithelial apical ridge and the underlying mesenchyme and also in the establishment of the dorso-ventral position of the ridge.

Fibronectin Type III Domain Containing 5 (Irisin) is a newly discovered hormone, secreted into circulation by muscle, which acts on white adipocytes and promotes WAT “browning”. r-Irisin can reduce body weight and cause induction of brown adipocyte in vivo, including a capacity for thermogenic energy expenditure mediated by uncoupling protein 1 (UCP-1). Irisin mature protein is comprised of 110 amino acid residues and two potential glycosylation sites. High levels of Irisin can be found in the heart whereas Very low expression is found in the colon, pancreas and spleen, if any.

GABARAPL2 takes part in intra Golgi traffic and modulates intra Golgi transport by coupling between NSF activity and SNAREs activation. GABARAPL2 first stimulates the ATPase activity of NSF which in turn stimulates the association with GOSR1.

Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 (CEACAM1) belongs to the carcinoembryonic antigen (CEA) gene family which is a part of the immunoglobulin superfamily. CEACAM1 is a cell adhesion protein which mediates homophilic cell adhesion in a calcium-independent way. CEACAM1 is a surface glycoprotein expressed on various blood cells, epithelial cells, and vascular cells. CEACAM1 functions as coinhibitory receptor in immune response, and plays a role also as an activator during angiogenesis.

Carcinoembryonic Antigen-Related Cell Adhesion Molecule 3, also known as CEACAM3, is a member of the immunoglobulin super family. The genes in this family encode cell adhesion proteins, which are expressed at higher levels in tumorous tissues rather than in normal tissues. CEACAM3 plays a significant part in the clearance of pathogens through the innate immune system. In addition, CEACAM3 is accountable for RAC1 stimulation in the course of pathogen phagocytosis.

Carcinoembryonic Antigen-Related Cell Adhesion Molecule 6 (CEACAM6) is a part of the human carcino-embryonic antigen (CEA) family. CEACAM6 belongs to the glycosylphosphatidylinositol-linked immunoglobulin superfamily which is involved in various human cancers. CEACAM6 is linked to the progression of pancreatic cancer.

Legumain, also known as LGMN is a lysosomal cysteine protease which is found in all mouse tissues, however it was mainly abundant in the kidney as well as placenta. LGMN plays an essential role in the endosomal/lysosomal degradation system as the Legumain deficiency causes the accumulation of pro cathepsins B, H & L, another group of lysosomal cysteine proteases. Furthermore, over expression of LGMN in tumors is important for invasion/metastasis.

Human thyrostimulin ranks among the glycoprotein hormone family. These hormones consist of two subunits, the common alpha- and specific beta-subunits, which associate noncovalently to form a heterodimer. The alpha-subunit combines with four distinct beta-subunits giving rise to four biologically active hormones in human: FSH, LH, TSH, and CG. FSH, LH, and TSH, mainly expressed in the anterior pituitary, are essential for coordinated endocrine regulation in the hypothalamus- pituitary axis and show to activate specific G protein–coupled receptors in the thyroid (TSH receptor) and gonads (LH and FSH receptors), respectively.
The heterodimeric glycoprotein hormones have only been identified in vertebrates and are highly conserved in organisms from primitive rayfin fish (Chondrostei) to human in both primary sequences and functional characteristics.
Corticotroph-derived glycoprotein hormone (CGH), also referred to as thyrostimulin, is a noncovalent heterodimer of glycoprotein hormone alpha 2 (GPHA2) and glycoprotein hormone beta 5 (GPHB5).
Recombinant A2/B5 heterodimeric glycoproteins activates human TSH receptors, but not LH and FSH receptors, and shows high affinity to TSH receptors in a radioligand receptor assay. The heterodimer also stimulates cAMP production and thymidine incorporation by cultured thyroid cells and increases serum thyroxine levels in TSH-suppressed rats in vivo. This new heterodimeric glycoprotein hormone was named as thyrostimulin based on its thyroid-stimulating activity. The expression of thyrostimulin in the anterior pituitary known to express TSH receptors suggested a paracrine mechanism.

WAP four-disulfide core domain protein 2 (WFDC2) is a protease inhibitor, which belongs to the WFDC domain family. WFDC2 is effective with a broad range of proteases, e.g. aspartic, serine or thiol proteases. WFDC2 is expressed in several normal tissues, including the male reproductive system, regions of the respiratory tract and nasopharynx. WFDC2 may be involved in sperm maturation. WFDC2 is also highly expressed in a number of tumors cells lines, such ovarian, colon, breast, lung and renal cells lines.

Alpha and Beta Defensins are cationic peptides with antimicrobial activity against Gram-negative and Gram-positive bacteria, fungi and enveloped viruses. These 2-6kDa proteins have vital roles in innate immune system. Mammalian Defensins are classified into alpha, beta and theta categories, based on their size and pattern of disulfide bonding. Beta-Defensins contain a six-cysteine motif which forms 3 intra-molecular disulfide bonds. Since beta-defensins are cationic peptides, they can therefore interact with the membrane of invading microbes, which are negative due to lipopolysaccharides (LPS) and lipoteichoic acid (LTA) found in the cell membrane. In addition, they can affect the stability of the membrane.

CRYGD is a member of the beta/gamma-crystallin family. Crystallins are the principal structural components of the vertebrate eye lens. The mammalian lens crystallins are divided into alpha, beta, and gamma families. Gamma-crystallins are involved in cataract formation. Defects in the CRYGD gene are responsible for cataract autosomal dominant (ADC), cataract congenital non-nuclear polymorphic autosomal dominant (CCP), cataract congenital cerulean type 3 (CCA3) and cataract crystalline aculeiform (CACA).

Migration And Invasion Enhancer 1 (MIEN1) is a member of the SelWTH family. MIEN1 enhances cell migration by stimulating filopodia formation at the leading edge of migrating cells and takes parts in regulation of apoptosis, probably via control of CASP3. MIEN1 participates in a redox-related process as well.

S100A6 is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs. S100 proteins are localized either in the cytoplasm or the nucleus of a wide range of cells. S100 proteins are involved in the regulation of a number of cellular processes such as cell cycle progression and differentiation. There are at least 13 members in the S100 gene family, which are located as a cluster on chromosome 1q21.
S100A6 may function in stimulation prolactin secretion, and exocytosis. Chromosomal rearrangements and altered expression of the S100A6 gene are implicated in melanoma.

Agouti-related protein is an endogenous antagonist of hypothalamic alpha-melanocortin receptors MC3R and MC4R with potent orexigenic activity. Although a complete deletion of the AGRP gene does not produce any significant metabolic phenotypes, reduction in AGRP expression by RNA interference is associated with increased metabolic rate along with reduced weight gain. In hypothalamus, it is produced by neurons in the medial portion of arcuate nucleus, which produce also the potent orexigenic peptide Neuropeptide Y (NP-Y). Another site of central AGRP production is the hypothalamic nucleus. AGRP encompasses 132 amino acid residues and its alpha-melanocortin inhibiting activity results in a 34 amino acid cystine knot domain within the C-terminal (87-132) portion of the protein. Both AGRP and NP-Y expression was shown to be suppressed by leptin. Central administration of AGRP induces hyperphagia and increased gain in body weight in rodents, but may also exert metabolic effects even when hyperphagia is prevented. In the absence of hyperphagia, intracerebralventricular administration of AGRP caused significant increases in plasma leptin and insulin concentrations (twofold and 1.5-fold, respectively) and fat pad mass.
In the periphery, AGRP mRNA was found in adrenal glands, lung, testis, ovary, skeletal muscle and adipose tissue in humans or rodents. In the adrenals, it was shown that AGRP antagonizes glucosteroid production mediated by MC4R. AGRP could then modulate locally the functions of some peripheral tissues such as adrenals.
In human and rat serum, detectable levels of AGRP-like activity were reported in the lower picogram range. The serum AGRP levels were elevated in obese humans compared to lean controls and increased with fasting in rats.

HINT1, also known as Histidine triad nucleotide-binding protein 1 is part of the superfamily named for a near C-terminal HXHXHXX motif (H:Histidine, X:a hydrophobic amino acid) positioned at the ?-phosphate of nucleotide substrates. HINT1 hydrolyzes adenosine 5'-monophosphoramidate substrates such as AMP-morpholidate, AMP-N-alanine methyl ester, AMP-alpha-acetyl lysine methyl ester and AMP-NH2. Though it was initially considered to be a protein kinase C inhibitor and act as a haplod-insufficient tumor suppressor including spontaneous tumor formation in Hint+/- and Hint-/- , its actual physiologic function is not known.

Homeodomain-only protein (HOPX) functions via its interaction with SRF, thus modulating the expression of SRF-dependent cardiac-specific genes and cardiac development. HOPX inhibits SRF-dependent transcription either by hindering SRF binding to DNA or by engaging histone deacetylase (HDAC) proteins which prevent transcription by SRF. HOPX is a homeodomain protein which lacks certain conserved residues required for DNA binding. HOPX overexpression causes cardiac hypertrophy.

ANXA2 is part of the annexin family and is involved in the regulation of cellular growth and in signal transduction pathways. ANXA2 protein functions as an autocrine factor which increases osteoclast formation and bone resorption. ANXA2 is associated with sickle cell osteonecrosis. Reduced ANXA2 expression is associated with osteosarcoma metastases. ANXA2 is part of the putative cell surface vitamin D binding protein binding site complex and functions to mediate the chemotactic cofactor effect. ANXA2 is involved in dysferlin deficiency and in muscular dystrophies. Human colon adenocarcinoma cell differentiation is related with an up-regulation of ANXA2.

ASF1 Anti-Silencing Function 1 Homolog B (ASF1B) belongs to the H3/H4 family of histone chaperone proteins and is similar to the anti-silencing function-1 protein in yeast. ASF1B is the substrate of the tousled-like kinase family of cell cycle-regulated kinases, and may have a crucial role in modulating the nucleosome structure of chromatin by guaranteeing a regular supply of histones at sites of nucleosome assembly. ASF1B cooperates with CAF-1 (chromatin assembly factor 1) to stimulate replication-dependent chromatin assembly. ASF1B is highly expressed in the testis and at lower levels in colon, small intestine and thymus. ASF1B is necessary for spermatogenesis.