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CISD1 protein holds a CDGSH iron-sulfur domain and is known to bind a redox-active [2Fe-2S] cluster. CISD1 is restricted to the outer membrane of mitochondria and takes part in oxidation regulation.

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.

PLGF is a growth factor active in angiogenesis, and endothelial cell growth, stimulating their proliferation and migration. It binds to receptor vegfr-1/flt1.

TNF-related apoptosis-inducing ligand (TRAIL) is a ligand molecule which induces apoptosis. It is a type II transmembrane protein with homology to other members of the tumor necrosis factor family.
In humans, the gene that encodes for TRAIL is located at chromosome 3q26.
TRAIL binds to the death receptors, DR4 and DR5. The process of apoptosis is caspase-8-dependent. This protein preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues.

Vascular endothelial growth factor (VEGF) is an important signaling protein involved in vessel formation As its name implies, VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells ). VEGF mediates increased vascular permeability, induces vasculogenesis and endothelial cell production, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor. VEGF is located in normal cartilage though only osteoarthritic cartilage expresses the VEGF receptors, NP1, VEGFR1 and VEGFR2. The VEGF level in the culture media from OA chondrocytes was more than 3 folds higher than in media from normal chondrocytes

Vascular endothelial growth factor is an important signaling protein involved in both vasculogenesis and angiogenesis. As its name implies, VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/ macrophagemigration, neurons, cancer cells, kidney epithelial cells ). VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesisand cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
Elevated levels of this protein are linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.

MGMT is an enzyme that repairs O-6-methylguanine, a mutagenic DNA base damaged by endogenous and environmental alkylating agents and takes part in the cellular defense against the biological effects of O-6-methylguanine in DNA. MGMT repairs alkylated guanine in DNA by stoichiometrically transferring the alkyl group at the O-6 position to a cysteine residue in the enzyme. abnormal MGMT expression correlates with the prognosis in human solid cancers. MGMT decrease of expression is correlated with methylation. The human MGMT is a negative regulator of estrogen receptor-mediated transcription upon alkylation DNA damage. MGMT promoter hypermethylation plays an important role in the early steps of colorectal carcinogenesis. Abnormal promoter hypermethylation of MGMT gene is associated with oral squamous cell carcinomas.

Vascular endothelial growth factor is an important signaling protein involved in both angiogenesis and vasculogenesis.VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells ).VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
Elevated levels of VEGF is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in VEGF have been associated with proliferative and nonproliferative diabetic retinopathy.

Hepatocyte Growth Factor (HGF) is a multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. HGF synergizes with Interleukin-3 and GM-CSF to stimulate colony formation of hematopoietic progenitor cells in vitro and may, therefore, also modulate hematopoiesis.

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.

Core 1 Beta3-Gal-T1 also known as,C1GALT1 creates the common core 1 O-glycan structure, Gal-beta-1-3GalNAc-R, by the transfer of Gal from UDP-Gal to GalNAc-alpha-1-R. Core 1 is a precursor for lots of extended mucin-type O-glycans on cell surface and secreted glycoproteins. Studies in mice have shown that this gene takes a main role in angiogenesis, thrombopoiesis and kidney homeostasis.

Penta-EF-hand domain containing 1 (PEF1) is a member of the penta-EF-hand protein family, which shares similarities to the apoptosis linked gene ALG-2. PEF1 forms heterodimers with PDCD6/ALG2 and dissociates from PDCD6/ALG2 in the presence of Ca (2+). Furthermore, PEF1 proteins bind calcium and participate in a various calcium-dependent processes in vertebrates.

PFN2 is a ubiquitous actin monomer-binding protein which is part of the profilin family. PFN2 regulates actin polymerization in response to extra cellular signals. PFN2 binds to actin and affects the structure of the cytoskeleton. At high concentrations, profilin prevents the polymerization of actin, while it increases it at low concentrations. PFN2 binds to PIP2, it inhibits the formation of IP3 and DG.

FSTL1 protein resembles follistatin, an activin-binding protein. FSTL1 is an autoantigen associated with rheumatoid arthritis and it holds an FS section, a follistatin-like sequence having 10 conserved cysteine residues.

CES1 is a part of the alpha/beta fold hydrolase familyand participates in the detoxification of xenobiotics and in the activation of ester and amide prodrugs. CES1hydrolyzes aromatic and aliphatic esters, although it has no catalytic activity toward amides or a fatty acyl-CoA ester. CES1hydrolyzes the methyl ester group of cocaine to form benzoylecgonine and catalyzes the transesterification of cocaine to form cocaethylene. CES1also plays a role in detoxification in the lung and protection of the central nervous system from ester or amide compounds.CES1 is found in most tissues, mainly in the liver.

CRNN is part of the "fused gene" family of proteins, which enclose N-terminus EF-hand domains and multiple tandem peptide repeats. CRNN contains two EF-hand Ca2+ binding domains in its N-terminus and two glutamine- and threonine-rich 60 amino acid repeats in its C-terminus. CRNN, also known as SEP53, which participates in the mucosal/epithelial immune response and epidermal differentiation. CRNN is a survival factor that participates in the clonogenicity of squamous esophageal epithelium cell lines, attenuates deoxycholic acid (DCA)-induced apoptotic cell death and discharge of calcium. When CRNN is over expressed in oral squamous carcinoma cell lines, it regulates negatively cell proliferation by the induction of G1 arrest.

Citrate synthase also known as CS is a Krebs tricarboxylic acid cycle enzyme which catalyzes the synthesis of citrate from oxaloacetate and acetyl coenzyme A. CS is present in almost all cells capable of oxidative metabolism. CS is nuclear encoded and transported into the mitochondrial matrix, where the mature form is found. The diseases related to CS are: critical illness polyneuropathy and mitochondrial cardiomyopathy.

CXC chemokine ligand 16 (CXCL16) is a type I membrane protein, which contains a non-ELR motif-containing CXC chemokine domain in its extracellular region. Human and Mouse CXCL16 share a 70% a.a. sequence similarity within their chemokine domains and 49% overall a.a. sequence identity. Functional CXCL16 can be dropped from the cell surface as an approximately 35kDa soluble protein. CXCR6 is the functional receptor for CXCL16. CXCL16 functions as a scavenger receptor on macrophages, which specifically binds to OxLDL (oxidized low density lipoprotein), proposing that CXCL16 may be involved in pathophysiology such as atherogenesis. In addition, CXCL16 induces a strong chemotactic response and calcium mobilization. CXCL16 binds to CXCR6/Bonzo.

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.

Stromal Cell-Derived Factor 2 (SDF2) is a secretory protein which is partly similar to the hydrophilic segments of yeast mannosyltransferases. SDF2 protein’s expression is ubiquitous and the gene is rather conserved among mammals. SDF2is a protein-coding gene whose alternative splicing results in coding and non-coding variants.

NADH dehydrogenase [ubiquinone] 1 alpha subcomplex assembly factor 4 (NDUFAF4) is involved in the compilation of mitochondrial NADH: ubiquinone oxidoreductase complex (complex I). In addition, NDUFAF4 is involved in cell proliferation and survival of hormone-dependent tumor cells. NDUFAF4 may also be a regulator of breast tumor cell invasion. NDUFAF4 gene mutations cause the mitochondrial complex I deficiency.

ASMT is a member of the methyltransferase superfamily. ASMT participates in melatonin biosynthesis. ASMT Expressed in brain, retina and pineal gland, ASMT utilities to catalyze the final reaction in the synthesis of melatonin, particularly the conversion of S-adenosyl-L-methionine and N-acetylserotonin to S-adenosyl-Lhomocysteine and melatonin.

EIF4EBP1 (eukaryotic translation initiation factor 4E-binding protein 1) belongs to a family of translation repressor proteins. EIF4EBP1 regulates eIF4E (eukaryotic translation initiation factor 4E) activity by preventing its assembly into the eIF4F complex and mediates the regulation of protein translation by hormones, growth factors and other stimuli that signal through the MAP kinase and mTORC1 pathways. EIF4EBP1 is phosphorylated in response to various signals including UV irradiation, resulting in its dissociation from eIF4E and activation of mRNA translation. EIF4EBP1 C-terminus has domains which control function and phosphorylation. EIF4EBP1 has a role in progression of breast neoplasms through cell signaling.

EIF4EBP2 belongs to the eukaryotic translation initiation factor 4E binding protein family. Even though EIF4EBP2 protein binds eIF4E and inhibits translation initiation, growth factors can release this inhibition by a phosphorylation-dependent disruption. EIF4EBP2 mediates the regulation of protein translation by hormones, growth factors and other stimuli that signal through the MAP kinase pathway. Regulation of this protein is associated to cell proliferation, cell differentiation and viral infection.