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Crk-like protein (CRKL) is a protein kinase containing SH2 and SH3 (src homology) domains which activates the RAS and JUN kinase signaling pathways and transforms fibroblasts in a RAS-dependent manner. CRKL is a substitute of the BCR-ABL tyrosine kinase, it also has a role in fibroblast transformation by BCR-ABL, and has oncogenic potential.

LRP2 Binding Protein (LRP2BP) is a protein coding gene which plays a role as an adapter that controls LRP2 function. LRP2BP is noticed in a vesicular staining pattern close to the plasma membrane and through the cytoplasm.

TOLLIP is a ubiquitin-binding protein that interacts with several Toll-like receptor (TLR) signaling cascade components. TOLLIP regulates inflammatory signaling and is involved in interleukin-1 receptor trafficking and in the turnover of IL1R-associated kinase.

C16ORF53 is a component of a Set1-like multiprotein histone methyltransferase complex. C16ORF53 interacts with PAXIP1/PTIP; this interaction is direct and is necessary for the association with the rest of the PTIP complex. The C16ORF53 protein has a crucial role in maintaining genome stability, condensation of chromatin and progression through mitosis.

GNAQ, also known as Guanine nucleotide-binding protein belong to the G-alpha family. Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in a variety of transmembrane signaling systems. GNAQ regulates B-cell selection and survival and is essential in order to prevent B-cell-dependent autoimmunity. GNAQ also regulates chemotaxis of BM-derived neutrophils and dendritic cells, in vitro. GNAQ is an alpha subunit in the Gq class, couples aseven-transmembrane domain receptor to activation of phospolipase C-beta. Mutations at this locus have beenconnected with problems in platelet activation and aggregation. A related pseudogene to GNAQ exists on chromosome 2.

The Argonaute protein is part of the RISC or RNA-induced silencing complex, as so, the protein has a key part in the slicing processes of RNA. The RNA interference (RNAi) is being held by RISC. Small non-coding RNA fragments bond to the Argonaute proteins, through base pairing, eventually leads to the cleavage of messenger RNA or translation suppression.

DNA/RNA-binding protein KIN17 (KIN17) is a nuclear protein which constructs intranuclear foci for the duration of proliferation and is reallocated in the nucleoplasm during the cell cycle. KIN17 is ubiqutiously expressed having the highest levels of expression in the muscle, heart and testis. SV40- altered fibroblasts overexpress KIN17, which interacts with Large T antigen and decreases T-antigen-dependent DNA replication.

Activins are homodimers or heterodimers of the different β subunit isoforms, part of the TGFβ family. Mature Activin A has two 116 amino acids residues βA subunits (βA-βA). Activin displays an extensive variety of biological activities, including mesoderm induction, neural cell differentiation, bone remodelling, haematopoiesis, and reproductive physiology. Activins takes part in the production and regulation of hormones such as FSH, LH, GnRH and ACTH. Cells that are identified to express Activin A include fibroblasts, endothelial cells, hepatocytes, vascular smooth muscle cells, macrophages, keratinocytes, osteoclasts, bone marrow monocytes, prostatic epithelium, neurons, chondrocytes, osteoblasts, Leydig cells, Sertoli cells, and ovarian granulosa cells.

Myeloid/Lymphoid Leukemia Translocated To 11 (MLLT11) is a part of the Mixed-Lineage Leukemia protein family. MLLT11 which takes part in leukemogenesis and in the progression of severe monocytic leukemia (AML) is located on chromosome 11q23. MLLT11 which is also expressed in embryonic brain cortex is upregulated during neuronal differentiation and is taking part in the evolution of the central nervous system.

KPNB1 is a member of the importin beta family. The KPNB1 protein is engaged in nuclear protein import, either by coupling itself with an adapter protein (e.g., importin-alpha subunit which binds to nuclear localization signals (NLS) in cargo substrates), or by functioning autonomously as a nuclear transport receptor (acts as NLS receptor, docking of the importin/substrate complex to the nuclear pore complex).

Suppressor of Cytokine Signaling 3, also known as SOCS3 belongs to the SOCS family; in addition SOCS3 is a member of the STAT-induced STAT inhibitor (SSI). The SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of SOCS3 is induced by different cytokines, including IL6 and IL10. SOCS3 can bind to JAK2 kinase, and inhibit the activity of JAK2 kinase. Studies of the mouse counterpart of SOCS3 have shown the roles of SOCS3 in the negative regulation of fetal liver hematopoiesis, and placental development.

HSP10 is part of the molecular chaperons, that are crucial for thir efficient folding of proteins in normal as well as stress conditions. GroES function is to bind to HSP60 in the presence of ATP, thus causing a change in the HSP60 conformation & enclosing the protein substrate within the complex. ATP hydrolysis by chaperonin-60 which destabilizes the HSP10-HSP60 complex, thereby allowing it to dissociate and secrete the substrate protein. GroES having the NCBI accession number of NP_002148 was purified by using conventional chromatography techniques.

ARF6 is a part of the ADP ribosylation factor family of GTP-binding proteins. ARF6 is restricted to the plasma membrane, and controls vesicular trafficking, remodeling of membrane lipids, and signaling pathways which lead to actin remodeling. Furthermore, ARF6 is a key player in conservation of organelle integrity, assembly of coat proteins and activation of phospholipase D.

Rho GDP-dissociation inhibitor 1 (ARHGDIA) is a member of the RAS gene superfamily, which encodes small guanine nucleotide exchange (GTP/GDP) factors. ARHGDIA, which is localized to the cytoplasm, inhibits the dissociation of GDP from Rho proteins, thus preventing GTP from binding to and consequently activating Rho proteins. In humans, the ARHGDIA can be phosphorylated at Ser 101 by p21-activated kinase, an event that inhibits its activity and may result in positive feedback regulation of several ARHGDIA target proteins.

TNFSF15 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is abundantly expressed in endothelial cells, but is not expressed in either B or T cells. The expression of TNFSF15 is inducible by TNF and IL-1 alpha. This cytokine is a ligand for receptor TNFRSF25 and decoy receptor TNFRSF21/DR6. It can activate NF-kappaB and MAP kinases, and acts as an autocrine factor to induce apoptosis in endothelial cells. TNFSF15 is also found to inhibit endothelial cell proliferation, and thus may function as an angiogenesis inhibitor. An additional isoform encoded by an alternatively spliced transcript variant has been reported but the sequence of this transcript has not been determined.

COMM Domain Containing (COMMD6) which is a part of the NF-kappa-B -inhibiting proteins, contains one COMM domain. COMMD6 down-regulates the activation of NF-kappa-B and inhibits TNF-induced NFKB1 activation.

Mitogen-activated protein kinase 1 (MAPK1) is also known as "extracellular signal-regulated kinase 2" (ERK2). Two similar (85% sequence identity) protein kinases were originally called ERK1 and ERK2. They were found during a search for protein kinases that are rapidly phosphorylated after activation of cell surface tyrosine kinasessuch as the epidermal growth factor receptor. Phosphorylation of ERKs leads to the activation of their kinase activity. The molecular events linking cell surface receptors to activation of ERKs are complex. It was found that RasGTP-binding proteins are involved in the activation of ERKs. Another protein kinase, Raf-1, was shown to phosphorylate a "MAPK kinase", thus qualifying as a "MAPK kinase kinase". The MAPK kinase was named "MAPK/ERK kinase" (MEK). Receptor-linked tyrosine kinases, Ras, Raf, MEK and MAPK could be fitted into a signaling cascade linking an extracellular signal to MAPK activation. Transgenic gene knockoutmice lacking MAPK1 have major defects in early development.

RAB18 belongs to a family of Ras-related small GTPase which is lipid-anchored to the cytoplasmic side of the cell membrane. RAB18 takes part in apical recycling, endocytosis and protein transport between early endosomes and the plasma membrane.

SUGT1 is homolog to yeast protein SGT1, a regulator of the cell cycle which is vital for G1/S and G2/M transitions. SUGT1 holds a CS domain, a SGS domain, a p23 domain and three tetratricopeptide repeats (TPR). SUGT1 protein associates with Skp1 p19 and CUL-1, subunits of the SCF ubiquitin ligase complex, and is believed to take a part in protein degradation. Furthermore, SUGT1 is essential for the kinetochores assembly, and has a role as a co-chaperone for HSP90.

Plasmodium falciparum heat shock proteins (PfHSPs) contribute to immunopathological alterations in infected hosts PfHSP70s may have a significant function during parasite adaptation in its environments. They have also been a focus of considerable attention due to their immunodominant antigenic nature and their properties as mediators of protective immunity.

SARS-Associated Coronavirus Nuclecapsid is an enveloped viral componentthat contains three external structural antigens, the mains are membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a membrenal receptor and mediates membrane fusion to grant viral entry into the target cells. therefore, S-protein has a crucial part in virus infection cycle and is the main target of neutralizing antibodies.

C1QBP having the accession number of NP_001203 binds to the globular "heads" of c1q thus inhibiting c1 activation. C1QBP interacts with a wide range of ligands and is implicated in cell signaling. C1QBP associates with C1r and C1s in order to yield the first component of the serum complement system. C1QBP protein has been identified as the p32 subunit of pre-mRNA splicing factor SF2, as well as a hyaluronic acid-binding protein.
C1QBP is a new marker of tumor cells and tumor-associated macrophages/myeloid cells in hypoxic/metabolically deprived areas of tumors.
Mitochondrial C1QBP is a critical mediator of p14ARF-induced apoptosis.
C1QBP functions as a chemotactic factor for immature dendritic cells, and migration is mediated through ligation of both C1QBP and cC1qR/CR.
C1QBP overexpression successfully blocks mRNA accumulation from the adenovirus major late transcription unit (MLTU) and stimulates RNA polymerase II carboxy-terminal domain phosphorylation in virus-infected cells.
C1QBP binds with Hepacivirus core protein on CD8+ and CD4+ positive t-cells and inactivates lck and akt.

Human immunodeficiency virus (HIV) is a retrovirusthat can lead to a condition in which the immune systembegins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the humanimmune systemsuch as helper T cells(specifically CD4+ T cells), macrophagesand dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytesthat recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Human immunodeficiency virus (HIV) is a retrovirusthat can lead to a condition in which the immune systembegins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the humanimmune systemsuch as helper T cells(specifically CD4+ T cells), macrophagesand dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytesthat recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.