proliferation

MAGOH (Mago Homolog, Exon Junction Complex Subunit) is a Protein Coding gene. MAGOH is the human homolog of Drosophila mago nashi, a protein that is required for normal germplasm development in the Drosophila embryo. In mammals, mRNA expression is not limited to the germplasm, but is expressed ubiquitously in adult tissues and can be induced by serum stimulation of quiescent fibroblasts. The exon junction complex (EJCs) are deposited on messenger RNAs (mRNAs) during splicing and their core consists of eIF4A3, MLN51, Y14, and MAGOH. Both MAGOH proteins interact with other EJC components, incorporate into mRNA-bound EJCs, and activate nonsense-mediated decay. Diseases associated with MAGOH include Metaphyseal Chondrodysplasia, Schmid Type, and Primary Autosomal Recessive Microcephaly.

MKI67 contains 1 FHA domain and plays a key role in cell proliferation. During interphase, the MKI67 antigen can be exclusively detected within the cell nucleus, whereas in mitosis most of the protein is relocated to the surface of the chromosomes. MKI67 protein is present during all active phases of the cell cycle (G1, S, G2, and mitosis), but is absent from resting cells. MKI67 is an excellent marker to determine the growth fraction of a given cell population. The fraction of MKI67-positive tumor cells is often correlated with the clinical course of cancer. It is also associated with ribosomal RNA transcription. Inactivation of antigen MKI67 leads to inhibition of ribosomal RNA synthesis. The MKI67 protein is a nuclear and nucleolar protein, which is tightly associated with somatic cell proliferation. Antibodies raised against the human MKI67 protein paved the way for the immunohistological assessment of cell proliferation, particularly useful in numerous studies on the prognostic value of cell growth in clinical samples of human neoplasms. MKI67 protein expression is an absolute requirement for progression through the cell-division cycle. Recently, MKI67 is proved to be an independent prognostic factor for disease-free survival (HR 1.5-1.72) in multivariate analyses studies using samples from randomized clinical trials with secondary central analysis of the biomarker. MKI67 was not found to be predictive for long-term follow-up after chemotherapy. Nevertheless, high KI-67 was found to be associated with immediate pathological complete response in the neoadjuvant setting, with an LOE of II-B. MKI67 could be considered as a prognostic biomarker for therapeutic decision.

NPDC1 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 16.9 kDa and the accession number is Q9NQX5.

May regulate the transport and translation of mRNAs of proteins involved in synaptic plasticity in neurons and cell proliferation and migration in multiple cell types. Binds directly and selectively to MYC and CCND2 RNAs. In neuronal cells, directly binds to several mRNAs associated with RNA granules, including BDNF, CAMK2A, CREB1, MAP2, NTRK2 mRNAs, as well as to GRIN1 and KPNB1 mRNAs, but not to rRNAs. Caprin-1/CAPRIN1 Protein, Human, Recombinant (His) is expressed in Baculovirus insect cells with N-10xHis tag. The predicted molecular weight is 80.7 kDa and the accession number is Q14444.

EBP1, also known as PA2G4, is an RNA-binding protein that belongs to the peptidase M24 family. It can be detected n several cell lines tested, including primary and transformed cell lines. EBP1 also present in pre-ribosomal ribonucleoprotein complexes and may be involved in ribosome assembly and the regulation of intermediate and late steps of rRNA processing. This protein is a transcriptional co-repressor of androgen receptor-regulated genes and other cell cycle regulatory genes through its interactions with histone deacetylases. PA2G4 can interact with the cytoplasmic domain of the ErbB3 receptor and may contribute to transducing growth regulatory signals. EBP1 has been implicated in growth inhibition and the induction of differentiation of human cancer cells. It seems to be involved in growth regulation. EBP1 also mediates cap-independent translation of specific viral IRESs (internal ribosomal entry site).

Tumor necrosis factor ligand superfamily member 13 belongs to the tumor necrosis factor family. It is also known as APRIL, TALL2, TRDL1, and CD256. It is synthesized as a 32 kDa proprotein which is cleaved by furin in the Golgi to release the active 17 kDa soluble molecule. TNFSF13 is a Cytokine that binds to TNFRSF13B/TACI and to TNFRSF17/BCMA and plays a role in the regulation of tumor cell growth. It expressed at high levels in transformed cell lines, cancers of colon, thyroid, lymphoid tissues and specifically expressed in monocytes and macrophages. Its expression by CD4+ T cells inhibits the production of Th2 cytokines and allergic inflammation.

Calcium-regulated non-lysosomal thiol-protease which catalyzes limited proteolysis of substrates involved in cytoskeletal remodeling and signal transduction. Proteolytically cleaves CTBP1 at 'Asn-375', 'Gly-387' and 'His-409'. CAPN1 Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 85.9 kDa and the accession number is P07384.

NCBP2 Protein, Human, Recombinant (GST) is expressed in E. coli expression system with N-GST tag. The predicted molecular weight is 44.9 kDa and the accession number is P52298.

Serpin H1 is a serine proteinase inhibitors Which belongs to the serpin family. Serpin H1 is induced by heat shock. Serpin H1 localizes to the endoplasmic reticulum lumen and binds specifically to collagen. Thus it is thought to be a molecular chaperone involved in the maturation of collagen molecules. Autoantibodies to this protein have been found in patients with rheumatoid arthritis. Serpin H1 may be a marker for cancer and nucleotide polymorphisms in this gene may be associated with preterm birth caused by preterm premature rupture of membranes.

TMX2 is a single-pass type I membrane protein and contains 1 thioredoxin domain. Thioredoxin plays an important role in various cellular processes through redox regulation. The Molecular Cloning and characterization of one member of the thioredoxin superfamily, designated as TMX2.The TMX2 cDNA consists of 1644 nucleotides and contains an open reading frame encoding a protein of 372 amino acids with a predicted molecular mass of 42.5 kDa and an isoelectric point of 8.94. The TMX2 protein may possess an N-terminal signal peptide, a potential transmembrane domain, an Myb DNA-binding domain repeat signature, a thioredoxin consensus pattern, an endoplasmic reticulum (ER) membrane retention signal (KKXX-like motif), and a dileucine motif in the tail.

Part of the endoplasmic reticulum membrane protein complex (EMC) that enables the energy-independent insertion into endoplasmic reticulum membranes of newly synthesized membrane proteins. Preferentially accommodates proteins with transmembrane domains that are weakly hydrophobic or contain destabilizing features such as charged and aromatic residues. Involved in the cotranslational insertion of multi-pass membrane proteins in which stop-transfer membrane-anchor sequences become ER membrane spanning helices. It is also required for the post-translational insertion of tail-anchored/TA proteins in endoplasmic reticulum membranes. By mediating the proper cotranslational insertion of N-terminal transmembrane domains in an N-exo topology, with translocated N-terminus in the lumen of the ER, controls the topology of multi-pass membrane proteins like the G protein-coupled receptors. By regulating the insertion of various proteins in membranes, it is indirectly involved in many cellular processes (Probable).

MKI67 Protein, Human, Recombinant (His) is expressed in Yeast.

Calcium-regulated non-lysosomal thiol-protease which catalyzes limited proteolysis of substrates involved in cytoskeletal remodeling and signal transduction. Proteolytically cleaves CTBP1 at 'Asn-375', 'Gly-388' and 'His-410'.

APRIL (a proliferation-inducing ligand), also known as TNFSF13, TALL2, TRDL1, and CD256, is a member of the TNF ligand superfamily. It is synthesized as a 32 kDa proprotein which is cleaved by furin in the Golgi to release the active 17 kDa soluble molecule. Secreted human APRIL, which consists almost entirely of a single TNF homology domain, shares 85% amino acid sequence identity with mouse and rat APRIL. Both APRIL and its close relative BAFF bind and signal through the TNF superfamily receptors TACI and BCMA, while BAFF additionally functions through BAFF R. APRIL binds to heparan sulfate proteoglycans (HSPGs) independently of its binding to TACI and BCMA. APRIL can form bioactive heterotrimers with BAFF, and these circulate in the serum of patients with rheumatic immune disorders. APRIL enhances the proliferation and survival of plasma cells and also promotes T cell-dependent humoral responses. APRIL levels are elevated in the serum during coronary artery disease, and it is also elevated in many cancers primarily due to expression by tumor-infiltratin neutrophils.

L-Lactate Dehydrogenase A Chain (LDHA) is an enzyme that catalyzes the conversion of L-lactate and NAD+ to pyruvate and NADH in the final step of anaerobic glycolysis. LDHA contains an N-terminal coenzyme binding region, a central catalytic site, and at least nine utilized Lys acetylation and two Tyr phosphorylation sites. LDHA belongs to the lactate dehydrogenase family, expressed predominantly in muscle tissue. LDHA mutations have been linked to exertional myoglobinuria.

Ferritin heavy polypeptide 1(FTH1), is a ubiquitous intracellular protein which stores iron in a soluble, non-toxic, readily available form. FTH1 has ferroxidase activity and is important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Ferritin is composed of 24 subunits of the light and heavy ferritin chains. It plays a role in delivery of iron to cells and mediates iron uptake in capsule cells of the developing kidney. Variation of ferritin subunit composition may affect iron absorption and release in different tissues. Deficiency of ferritin proteins may cause several neurodegenerative diseases. Almost all living organisms can produce this protein, including algae, bacteria, higher plants, and animals.

MKI67 Protein, Human, Recombinant (E. coli, His) is expressed in E. coli.

Involved in the uptake of thrombin-antithrombin complexes by hepatic cells. When phosphorylated, plays a role in filament reorganization. Involved in the delivery of mutated CFTR to the plasma membrane. Together with KRT8, is involved in interleukin-6 (IL-6)-mediated barrier protection. KRT18 Protein, Human, Recombinant (E. coli, His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 52.0 kDa and the accession number is P05783.

Involved in the uptake of thrombin-antithrombin complexes by hepatic cells. When phosphorylated, plays a role in filament reorganization. Involved in the delivery of mutated CFTR to the plasma membrane. Together with KRT8, is involved in interleukin-6 (IL-6)-mediated barrier protection.

Plays a role in promoting the proliferation of synovial fibroblasts in response to proinflammatory stimuli.

KMT5A (known as PR-Set7/9, SETD8 and SET8), a member of the SET domain containing methyltransferase family specifically targeting H4K20 for methylation, has been implicated in multiple biological processes. Inhibition of KMT5A attenuated proliferation and induced apoptosis. Elevated KMT5A expression was significantly correlated with extrathyroidal extension, lymph node metastasis and advanced pathological stage of papillary thyroid cancer. KMT5A may be a novel oncogenic factor, specifically a regulator for lipid metabolism in papillary thyroid carcinoma.

Integrin-linked kinase-associated serine/threonine phosphatase 2C, also known as ILKAP, is a cytoplasm protein that belongs to the PP2C family. ILKAP contains one PP2C-like domain. ILKAP is widely expressed. Highest levels expressed in striated muscle. Much lower levels are evident in various smooth muscle tissues. ILKAP may play a role in the regulation of cell cycle progression via dephosphorylation of its substrates whose appropriate phosphorylation states might be crucial for cell proliferation. ILKAP selectively associates with integrin-linked kinase (ILK), to modulate cell adhesion and growth factor signaling. ILKAP inhibits the ILK-GSK3B signaling axis and may play an important role in inhibiting oncogenic transformation. Integrin-linked kinase ( ILK ) plays key roles in a variety of cell functions, including cell proliferation, adhesion, and migration. Within the cell, ILK localizes to multiple sites, including the cytoplasm, focal adhesion complexes that mediate cell adhesion to extracellular substrates, as well as cell-cell junctions in epidermal keratinocytes. Nuclear ILK can be rapidly exported into the cytoplasm through a CRM1-dependent pathway, and its export is enhanced by the type 2C protein phosphatase ILKAP. Nuclear localization of ILK in epidermal keratinocytes is associated with increased DNA synthesis, which is sensitive to inhibition by ILKAP.

Aldehyde dehydrogenase 3A1 (ALDH3A1) is a metabolic enzyme that catalyzes the oxidation of various aldehydes. Certain types of epithelial tissues in mammals, especially those continually exposed to environmental stress (e.g., corneal epithelium), express ALDH3A1 at high levels and its abundance in such tissues is perceived to help to maintain cellular homeostasis under conditions of oxidative stress. Metabolic as well as non-metabolic roles for ALDH3A1 have been associated with its mediated resistance to cellular oxidative stress. Aldehyde dehydrogenase 1A1 (ALDH1A1) and ALDH3A1 are corneal crystallins. They protect inner ocular tissues from ultraviolet radiation (UVR)-induced oxidative damage through catalytic and non-catalytic mechanisms. Additionally, ALDH3A1 has been postulated to play a regulatory role in the corneal epithelium based on several studies that report an inverse association between ALDH3A1 expression and corneal cell proliferation. Aldehyde dehydrogenase 3A1 (ALDH3A1) plays an important role in many cellular oxidative processes, including cancer chemoresistance, by metabolizing activated forms of oxazaphosphorine drugs such as cyclophosphamide (CP) and its analogues, such as mafosfamide (MF), ifosfamide (IFM), and 4-hydroperoxycyclophosphamide (4-HPCP). Compounds that can selectively target ALDH3A1 could permit delineation of its roles in these processes and could restore chemosensitivity in cancer cells that express this isoenzyme. ALDH3A1 may act to protect corneal cells against cellular oxidative damage by metabolizing toxic lipid peroxidation products (e.g., 4-HNE), maintaining cellular GSH levels and redox balance, and operating as an antioxidant.

PTMA (prothymosin, alpha, N-GST chimera) is a small, 12.4 kDa protein. It is a 109-111 amino acid long polypeptide as the precursor of thymosin a1. Thymosins are named becaues they were originally isolated from the thymus. But now in many other tissues, thymosins also can be detected. Thymosins have diverse biological activities, and two in particular, thymosins a1 and _4, have potentially important uses in medicine, some of which have already progressed from the laboratory to the clinic. In general, PTMA is associated with cellular proliferation and carcinogenesis (Eschenfeldt et al., 1986), cellular and viral transcription (Cotter et al., 2000), protection against apoptosis and chromatin remodelling (Karetsou et al., 1998). PTMA may have a dual role both intracellulary and extracellulary. In relation to diseases, thymosins have been categorized as biological response modifiers. Thymosin a1 is derived from PTMA. For animals that lack thymus glands, thymosin a1 is responsible for the activity of that preparation in restoring immune function.

Claudin-11, also known as CLDN11, belongs to the group of claudins. Claudins are integral membrane proteins and components of tight junction strands. Tight junction strands function as a physical barrier to prevent solutes and water from passing freely through the paracellular space between epithelial or endothelial cell sheets, and also play critical roles in maintaining cell polarity and signal transductions.Claudin-11 is a tight junction associated protein and is a major component of central nervous system (CNS) myelin that is necessary for normal CNS function. Human blood-testis barrier disruption is related to a dysfunction of CLDN11 gene. It plays an important role in regulating proliferation and migration of oligodendrocytes.

The histone chaperone anti-silencing factor 1a (ASF1a) interacts with MDC1 and is recruited to sites of DSBs to facilitate the interaction of phospho-ATM with MDC1 and phosphorylation of MDC1, which are required for the recruitment of RNF8/RNF168 histone ubiquitin ligases. Thus, ASF1a deficiency reduces histone ubiquitination at DSBs, decreasing the recruitment of 53BP1, and decreases NHEJ, rendering cells more sensitive to DSBs. This role of ASF1a in DSB repair cannot be provided by the closely related ASF1b and does not require its histone chaperone activity. Homozygous deletion of ASF1A is seen in 10%-15% of certain cancers, suggesting that loss of NHEJ may be selected in some malignancies and that the deletion can be used as a molecular biomarker for cancers susceptible to radiotherapy or to DSB-inducing chemotherapy. Anti-silencing function 1 (ASF1) is a histone H3-H4 chaperone involved in DNA replication and repair, and transcriptional regulation. Here, we identify ASF1B, the mammalian paralog to ASF1, as a proliferation-inducing histone chaperone in human β-cells. Overexpression of ASF1B led to distinct transcriptional signatures consistent with increased cellular proliferation and reduced cellular death.

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.

Chemokine (C-X-C motif) ligand 17 (CXCL17) is the latest member of the chemokine family. CXCL17 is a potential oncogene and promising therapeutic target, is an independent biomarker of poor prognosis in patients with breast cancer, and can promote proliferation and migration of breast cancer cells in vitro and in vivo. CXCL17 is expressed in a variety of cancers and promotes tumor progression by recruiting myeloid-derived suppressor cells (MDSCs). CXCL17 attenuates IMQ-induced psoriasis-like skin inflammation by recruiting MDSCs and Tregs, which may be important for regulating excessive inflammation in psoriasis skin. CXCL17 production correlated with adverse immune infiltration and might be an important target for anti-HCC therapies. CXCL17 is a major regulator of mucosal inflammatory responses.

Platelet-derived growth factor alpha (PDGFA) is frequently upregulated in various cancers and thought to function as a key player in the development and progression of tumor growth by regulating aspects of cell proliferation, angiogenesis and metastasis. The human platelet-derived growth factor A chain gene (PDGFA) on chromosome 7p22 encodes an important mitogen. Within PDGFA lies a complex minisatellite structure that results in partial duplications of exon 4 and the IVS4 splice donor site. PDGFA Protein, Rat, Recombinant (His) is expressed in yeast with His tag. The predicted molecular weight is 14.5 kDa and the accession number is AAB26134.2.

Platelet-derived growth factor alpha (PDGFA) is frequently upregulated in various cancers and thought to function as a key player in the development and progression of tumor growth by regulating aspects of cell proliferation, angiogenesis and metastasis. The human platelet-derived growth factor A chain gene (PDGFA) on chromosome 7p22 encodes an important mitogen. Within PDGFA lies a complex minisatellite structure that results in partial duplications of exon 4 and the IVS4 splice donor site. PDGFA Protein, Canine, Recombinant (His) is expressed in yeast with His tag. The predicted molecular weight is 14.5 kDa and the accession number is A0A8C0M6T8.

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.

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.

Serpins are the largest and most diverse family of serine protease inhibitors which are involved in a number of fundamental biological processes such as blood coagulation, complement activation, fibrinolysis, angiogenesis, inflammation and tumor suppression and are expressed in a cell-specific manner. Serpins are a group of proteins with similar structures that were first identified as a set of proteins able to inhibit proteases. The acronym serpin was originally coined because many serpins inhibit chymotrypsin-like serine proteases (serine protease inhibitors). Over 1 serpins have been identified.Mouse SerpinB1, also known as Peptidase inhibitor 1, PI-1, Bomapin and SERPINB1, is a nucleus and cytoplasm protein that belongs to the serpin family and Ov-serpin subfamily. SerpinB1 is expressed specifically in the bone marrow. SerpinB1 is a protease inhibitor that may play a role in the regulation of protease activities during hematopoiesis and apoptosis induced by TNF. SerpinB1 is a redox-sensitive nuclear serpin that augments proliferation or apoptosis of leukaemia cells, depending on growth factors availability. SerpinB1 may regulate protease activities in the cytoplasm and the nucleus.

RCAS1, also known as EBAG9, is a tumor-associated antigen that is expressed at high frequency in a variety of cancers. RCAS1 gene was identified as an estrogen-responsive gene. Regulation of transcription by estrogen is mediated by estrogen receptor which binds to the estrogen-responsive element (ERE) found in the 5'-flanking region of RCAS1 gene. Two transcript variants differing in the 5' UTR, but encoding the same protein, have been identified for RCAS1 gene. EBAG9 may participate in suppression of cell proliferation and induces apoptotic cell death through activation of interleukin-1-beta converting enzyme (ICE)-like proteases.

ING4 is similar to ING1, a tumor suppressor protein that can interact with TP53, inhibit cell growth, and induce apoptosis. ING4 contains a PHD-finger, which is a common motif in proteins involved in chromatin remodeling. ING4 protein can bind TP53 and EP3/p3, a component of the histone acetyltransferase complex, suggesting its involvement in the TP53-dependent regulatory pathway. ING4 is a component of the HBO1 complex which has a histone H4-specific acetyltransferase activity, a reduced activity toward histone H3 and is responsible for the bulk of histone H4 acetylation in vivo. Through chromatin acetylation, it may function in DNA replication. ING4 may also inhibit tumor progression by modulating the transcriptional output of signaling pathways that regulate cell proliferation.

BIRC5, also known as Survivin and EPR-1, is a member of theIAP family. IAP family members usually contain multiple baculovirus IAP repeat (BIR) domains, but BIRC5 has only a single BIR domain. It is expressed cell cycle-dependently and highly expressed at mitosis. As a multitasking protein, BIRC5 has dual roles in promoting cell proliferation and preventing apoptosis. Survivin is a component of a chromosome passage protein complex (CPC) which is essential for chromosome alignment and segregation during mitosis and cytokinesis. Survivin acts as an important regulator of the localization of this complex. It may counteract a default induction of apoptosis in G2/M phase.

Eukaryotic translation initiation factor 5A2 (EIF5A2) has been demonstrated to be upregulated in numerous types of human cancer and is associated with cancer progression. Silencing of EIF5A2 in the NSCLC cells resulted in the downregulation of the tumorigenic proteins, apoptosis regulator Bcl-2 and myc proto-oncogene protein, and upregulation of E-cadherin, suggesting that EIF5A2 promotes proliferation and metastasis through these proteins. EIF5A2 may therefore serve as a novel therapeutic target for the treatment of NSCLC. EIF5A2 might be a novel therapeutic target for the inhibition of NPC progress. EIF5A2 overexpression may contribute to cancer progression and poor prognosis, it could be a novel potential prognostic marker for FIGO stage I-II cervical cancer. EIF5A2 upregulation plays an important oncogenic role in gastric cancer. EIF5A2 may represent a new predictor for poor survival and is a potential therapeutic target for gastric cancer. The eukaryotic initiation factor 5A2 (EIF5A2) over-expression enhances HCC cell metastasis. EIF5A2, as a target of PI3K/Akt, promotes melanoma cell invasion and may serve as a promising prognostic marker and a potential therapeutic target for melanoma.

Ribosomal protein S6 kinase alpha-2, also known as 9 kDa ribosomal protein S6 kinase 2, MAP kinase-activated protein kinase 1c, MAPK-activated protein kinase 1c, Ribosomal S6 kinase 3, RSK-3, RPS6KA2 and MAPKAPK1C, is a nucleus protein that belongs to the protein kinase superfamily, AGC Ser/Thr protein kinase family and S6 kinase subfamily. RPS6KA2 / RSK-3 is expressed in many tissues. Highest expression is in lung and skeletal muscle. The expression of RPS6KA2 reduced proliferation, caused G1 arrest, increased apoptosis, reduced levels of phosphorylated extracellular signal-regulated kinase and altered other cell cycle proteins. RPS6KA2 / RSK-3 contains one AGC-kinase C-terminal domain and two protein kinase domains. It forms a complex with either ERK1 or ERK2 in quiescent cells. It transiently dissociates following mitogenic stimulation. RPS6KA2 / RSK-3 is a serine/threonine kinase that may play a role in mediating the growth-factor and stress induced activation of the transcription factor CREB. RPS6KA1, RPS6KA2, RPS6KB1, RPS6KB2, and PDK1 are involved in several pathways central to the carcinogenic process, including regulation of cell growth, insulin, and inflammation.

Mitogen-activated protein kinase 8 (MAPK8), also known as JNK1, is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation, and development. The protein kinases JNK1 has been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. It is critically involved in the promotion of diet-induced obesity, metabolic inflammation, and beta-cell dysfunction. The selective deficiency of JNK1 in the murine nervous system is sufficient to suppress diet-induced obesity. Genetic analysis indicates that the effects of JNK1 can be separated from the effects of JNK1 on obesity. JNK1 is a potential pharmacological target for the development of drugs that might be useful for the treatment of metabolic syndrome, and type 2 diabetes. Furthermore, JNK1 plays a major role in hypoxic cellular damage. JNK1 protein might be an attractive target for anti-hypoxic therapy in increasing resistance to many pathological conditions and diseases, leading to the oxygen deficit.

PS6K, also known as RPS6KB1, is a serine/threonine-protein kinase. It belongs to the RSK (ribosomal s6 kinase) family. Members of this family function in signal transduction. PS6K is an isoform of p70 ribosomal S6 kinase (S6K). S6K can be activated by mitogenic stimuli such as growth factors, insulin and cytokines. It phosphorylates the ribosomal protein S6. PS6K also phosphorylates other proteins such as elF4B, eEF2K and SKAR. It is a crucial effector of mTOR(rapamycin) signaling. PS6K is dissociated from the EIF3 complex and activated upon mitogenic stimulation, phosphorylation by the mammalian target of mTOR complex 1 (mTORC1). Its active form then phosphorylates and activates several substrates in the preinitiation complex, including the EIF2B complex and the cap-binding complex component EIF4B. PS6K also functions in cell proliferation, cell growth and cell cycle progression.

FGF (fibroblast growth factor) signalling is known to be required for many aspects of mesoderm formation and patterning during Xenopus development and has been implicated in regulating genes required for the specification of both blood and skeletal muscle lineages. Fibroblast growth factor 4 (FGF4) signaling induces differentiation from embryonic stem cells (ESCs) via the phosphorylation of downstream molecules such as mitogen-activated protein kinase/extracellular signal-related kinase (MEK) and extracellular signal-related kinase 1/2 (ERK1/2). Fibroblast Growth Factor 4 (FGF-4) could not only increase the proliferation of bone marrow mesenchymal stem cells (BMSCs), but also induce BMSCs into hepatocyte-like cells in vitro. FGF4 transduced BMSCs contributed to liver regeneration might by the transplanted microenvironment. The FGF4-bFGF BMSCs thus can enhance the survival of the transplanted cells, diminish myocardial fibrosis, promote myocardial angiogenesis, and improve cardiac functions.

Interleukin 11 (IL-11) is a member of a family of human growth factors that includes human growth hormone, granulocyte colony-stimulating factor, and other growth factors. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. It also promotes the proliferation of hepatocytes in response to liver damage. Binding to its receptor formed by IL6ST and either IL11RA1 or IL11RA2, It activates a signaling cascade that promotes cell proliferation. The signaling leads to the activation of intracellular protein kinases and the phosphorylation of STAT3.

Growth-regulated alpha protein (CXCL1,KC), is a member of the alpha chemokine subfamily, was initially identified as an immediate early gene induced in mouse fibroblasts by platelet-derived growth factor. The N-terminal processed form KC(5-72) of the protein is produced by proteolytic cleavage after secretion from bone marrow stromal cells, and shows a highly enhanced hematopoietic activity. Mouse KC shows approximately 63% identity to that of mouse MIP-2. KC is also approximately 60% identical to the human GROs. It has been suggested that mouse KC and MIP-2 are the orthologs of the human GROs and rat CINCs. Cxcl1 has chemotactic activity for neutrophils, and contributes to neutrophil activation during inflammation. Hematoregulatory chemokine, in vitro, suppresses hematopoietic progenitor cell proliferation.

Galectin-1 is a member of growing family of evolutionary conserved animal lectins. Galectin-1 is widely expressed in many cells and tissues. Galectins consists of a Galectin domain and two Beta-galactoside binding domains. Galectin-1 can binds LGALS3BP and interacts with CD2, CD3, CD4, CD7, CD43 and CD45. Galectin-1 may act as an autocrine negative growth factor which regulates apoptosis, cell proliferation and cell differentiation. In addition, Galectin-1 plays improtant roles in immunosuppressive and antiinflammatory properties.

Interleukin 3 is a pleiotropic factor produced primarily by activated T cells that can stimulate the proliferation and differentiation of pluripotent hematopoietic stem cells as well as various lineage committed progenitors. In addition, IL-3 also affects the functional activity of mature mast cells, basophils, eosinophils and macrophages.Because of its multiple functions and targets, it was originally studied under different names, including mast cell growth factor P-cell stimulating factor, burst promoting activity, multi-colony stimulating factor, thy-1 inducing factor and WEHI-3 growth factor. In addition to activated T cells, other cell types such as human thymic epithelial cells, activated mouse mast cells, mouse keratinocytes and neurons/astrocytes can also produce IL-3. IL-3 exerts its biological activities through binding to specific cell surface receptors. The high affinity receptor responsible for IL-3. signaling is composed of α and βsubunits. IL-3 is capable of supporting the proliferation of abroad range of hematopoietic cell types. It is involved in avariety of cell activities such as cell growth, differentiation and apoptosis. IL-3 has been shown to also possess neurotrophic activity, and it may be associated with neurologic disorders.

Human Chemokine (C-C Motif) Ligand 3 (CCL3) is a small cytokine belonging to the CC chemokine family. CCL3 is primarily expressed in T cells, B cells, and monocytes after antigen or mitogen stimulation. CCL3 exhibits chemoattractive and adhesive effects on lymphocytes. CCL3 exerts multiple effects on hematopoietic precursor cells and inhibits the proliferation of hematopoietic stem cells in vitro as well as in vivo. CCR1 and CCR5 have been identified as functional receptors for CCL3.

B-cell activating factor (BAFF), also known as BLyS, TALL-1, THANK, and TNFSF13B, is a transmembrane glycoprotein in the TNF ligand superfamily. BAFF is a cytokine and serves as a ligand for receptors TNFRSF13B (TACI), TNFRSF17 (BCMA), and TNFRSF13C (BAFFR). BAFF can promotes the survival, proliferation and maturation of B lymphocytes, which are key elements in the pathogenesis of systemic lupus erythematosus (SLE). This cytokine is encoded on TNFSF13B gene, and diverse single-nucleotide polymorphisms have been associated with susceptibility in diferent autoimmune disorders. BAFF is a transmembranal protein expressed on myeloid lineage and some epithelial cells, through diferent stimuli such as IFN-γ, IFN-α, interleukin (IL)-10, Toll-like receptors (TLR)-3, TLR-4 and TLR-7.

Follistatin-Related Protein 1 (FSTL1) is a secreted protein that contains two EF-hand domains, one follistatin-like domain, one Kazal-like domain, and one VWFC domain. Its functional significance in physiological and pathological processes is not completely understood. However, FSTL1 is thought to modulate the action of some growth factors on cell proliferation and differentiation. FSTL1 maybe an autoantigen associated with rheumatoid arthritis.

Tumor necrosis factor receptor superfamily member 9(TNFRSF9) is a member of the tumor necrosis factor (TNF) receptor family. It can be induced by lymphocyte activation (ILA) and is expressed by activated T cells, but to a larger extent on CD8 than on CD4 T cells. In addition, TNFRSF9 expression is found on dendritic cells, follicular dendritic cells, natural killer cells, granulocytes and cells of blood vessel walls at sites of inflammation. As receptor for TNFSF9/4-1BBL, it can activate T cells and the cross-linking of this protein can enhance T cell proliferation, IL-2 secretion survival and cytolytic activity. Further, it can enhance immune activity to eliminate tumors in mice.

Activin Receptor-Like Kinase 1 (ALK-1) is a type I cell-surface receptor for the TGF-β superfamily of ligands, which mediates signaling of BMP9 (bone morphogenetic protein) and BMP10. ALK1 signaling is necessary for angiogenesis during embryogenesis, wound healing, and tumor growth. ALK-1 has a high degree of similarity in serine-threonine kinase subdomains, a glycine and serine rich region preceding the kinase-domain, and a C-terminal tail with other activin receptor-like kinase proteins. ALK-1 is mainly expressed in endothelial cells regulating proliferation and migration in vitro and angiogenesis in vivo. Mutations in ALK-1 as well as in endoglin are associated with hereditary hemorrhagic telangiectasia (HHT), suggesting ALK-1 plays a critical role for in the control of blood vessel development or repair.