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NANOGP8 belongs to the homeobox family of DNA binding transcription factors which is known to conserve pluripotency of embryonic stem cells. One change only separate NANOGP8 from NANOG – instead of 'Gln-253' in the inferred amino acid sequence in NANOG there is a ‘His-253’ in NANOGP8.

C9 binds to the C5b-8 complex and formson cell membranes the mature membrane attack complex. Each pathway of complement activation generates proteolytic enzyme complexes which binds the target surface. These enzymes cleave a peptide bond in the larger alpha chain of C5 releasing the anaphylatoxin C5a and activating C5b. This is the only proteolytic step in the assembly of the C5b-9 complex. Although C5b is unstable it remains bound to the activating complex for a few minutes during which it binds a single C6 from the surrounding fluid or it decays and is no longer capable of forming MAC.The C5b,6 complex may also remain connected to the C3/C5 convertase where the binding of a single C7 exposes a membrane-binding region and C5b,6,7 can enter into the bilipid layer of the target cell. Each C5b-7 complex can bind 1 molecule of C8 causing the complex to enter more firmly into the membrane. The C5b-8 complex can cause lysis without C9,though it will take longer andwill require many more complexes per cell than with C9. The main role of C8 is to catalyze the binding of C9 and each can bind another C9 initiating formation of a ring structure containing up to 18 C9molecules.C5b-9 complexes with 1 or more C9 are called the Membrane Attack Complex of complement.

The gamma globin genes which are HBG1 and HBG2, usually expressed in the fetal liver, spleen and bone marrow. 2 gamma chains together along with 2 alpha chains comprise fetal hemoglobin (HbF) which is normally replaced by mature hemoglobin (HbA) at birth. Gamma chain production continues into adulthood in several beta-thalassemias and linked situations. The two types of gamma chains differ at residue 136 where glycine is found in the G-gamma product (HBG2) and alanine is found in the A-gamma product (HBG1). The former is predominant at birth.

Sialic Acid Binding Ig Like Lectin 10(SIGLEC10) is a part of the immunoglobulin superfamily that is expressed on eosinophils, B cells, monocytes and neutrophils. SIGLEC10 is an adhesion molecule that mediates sialic-acid dependent binding to cells.SIGLEC10 is a ligand for CD52, the target of the therapeutic monoclonal antibody Alemtuzumab. Also, it binds to Vascular adhesion protein 1 (VAP-1) and to the co-stimulatory molecule CD24.This binding is modulated by cis interactions of SIGLEC10 with sialated molecules on the same cell.

PRDX3 is part of the peroxiredoxin family of antioxidant enzymes, that reduces hydrogen peroxide and alkyl hydroperoxides. PRDX3 is particularly located in the mitochondria and involved in the regulation of cellular redox status by serving as a primary line of defense against H2O2 produced during respiration. PRDX3 is a significant regulator of the abundance of mitochondrial H(2)O(2), which itself promotes apoptosis in cooperation with other mediators of apoptotic signaling. PRDX3 mitochondrial protein is significantly decreased in Alzheimer Disease and Down Syndrome.

BETV4 is primarily expressed in mature birch (Betula verrucosa) pollen and Causes an allergic reaction in human. BETV4 is a calcium-binding protein of 2-EF-hand type, which is exists in pollen of various plant species. This cross-reactivity can serve as a marker allergen for plant polysensitization.

Tetratricopeptide repeat protein 33 (TTC33) is comprised of 3 TPR repeats.

The cytokine Macrophage migration inhibitory factor (MIF) has been identified to be secreted by the pituitary gland and the monocyte/macrophage and to play an important role in endotoxic shock. MIF has the unique property of being released from macrophages and T cells in response to physiological concentrations of glucocorticoids. The secretion of MIF is tightly regulated and decreases at high, anti-inflammatory steroid concentration.

RAB, Member RAS Oncogene Family-Like 5 (RABL5) belongs to the Ras superfamily of small GTP-binding proteins. The Ras-related superfamily of guanine nucleotide binding proteins includes the R-Ras, Rap, Ral/Rec and Rho/Rab subfamilies. Rab proteins have an essential role in endocytosis or in biosynthetic protein transport. The transporting process of newly synthesized proteins from the endoplasmic reticulum to various stacks of the Golgi complex and to secretory vesicles includes the movement of carrier vesicles and requires Rab protein function.

Zinc-alpha-2-glycoprotein (ZAG) is found in body fluids such as serum, sweat, and seminal and breast cyst fluids. It is identical in amino acid sequence to tumor-derived lipid mobilizing factor (LMF), a protein associated with the dramatic loss of adipose body stores in cancer cachexia, and has been shown to stimulate lipolysis by adipocytes in vivo and in vitro. A role for ZAG has been proposed in the regulation of body weight, and age-dependent changes in genetically influenced obesity, and also it regulates melanin production by normal and malignant melanocytes. It has also recently been classified as a novel adipokine in that it is produced by both white and brown fat adipocytes and may act in a local autocrine fashion in the reduction of adiposity in cachexia. Controlling ZAG/LMF's activity could be life-saving in the management of certain cancers and other cachexiainducing conditions, and its possible normal role in body fat store homeostasis is deserving of understanding in its own right. ZAG exhibits a class I major histocompatibility complex (MHC) fold but is a soluble protein rather than being anchored to plasma membranes and does not associate with alpha-2-microglobulin in humans. Like antigen-presenting MHC class I proteins, ZAG has an open apical groove, and X-ray crystallography of human derived ZAG revealed an unidentifiable electron density in a similar position to that occupied by antigenic peptides in classical MHC proteins and glycolipids in isoforms of CD1. This presumptive ligand is not a peptide, and the groove is too small to hold a glycolipid such as is presented by CD1 isoforms. By analogy with all other MHC class I-related proteins that have an open apical groove [some do not ], occupancy by a ligand is probably crucial to ZAG's biological function. Despite all of the structural and biochemical evidence that ZAG binds a ligand, none has so far been found by extraction from protein isolated from biological fluids. This difficulty could be because the ligand is labile, heterogeneous, or readily lost during purification procedures. Knowing more about how ZAG interacts with the compounds it has been found to bind, both natural and artificial, will inform searches for the elusive ligand(s) and its/their role in ZAG's signaling function.

Signal-Regulatory Protein Alpha, SIRPA belongs to the signal-regulatory-protein (SIRP) family, as well as theimmunoglobulin super family. The members of the SIRP family are receptor-type transmembrane glycoproteins which areinvolved in the negative regulation of receptor tyrosine kinase-coupled signaling processes. SIRPA can bephosphorylated by tyrosine kinases. The phospho-tyrosine residues of this PTP have been shown to recruit SH2domain containing tyrosine phosphatases (PTP), and perform as substrates of PTPs. SIRPA take part insignal transduction mediated by a variety of growth factor receptors. CD47 has been shown to be a ligand for SIRPA.

The acute phase plasma protein ORM1 synthesized by the liver mediates the interaction between blood cells and endothelial cells. In addition, together with haptoglobin and C reactive protein, ORM1 regulates the extravasation of the cells through infection and inflammation. Expression of ORM1 is induced by acute-phase stimulatory mediators such as bacterial lipopolysaccharides.

Recombinant Fatty Acid Binding Protein is a newly introduced plasma marker of acute myocardial infarction (AMI). The plasma kinetics of FABP (15kD) closely resemble those of myoglobin in that elevated plasma concentrations are found within 2 hours after AMI and return to normal generally within 18 to 24 hours. But the concentration of FABP in the skeletal muscle is 20 times lower than in cardiac tissue (for myoglobin the same content for cardiac and skeletal tissue), that makes FABP to be more cardiac specific than myoglobin. This makes FABP a useful biochemical marker for the early assessment or exclusion of AMI. FABP also appears to be a useful plasma marker for the estimation of myocardial infarct size.

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.

Troponin I, fast skeletal muscle (TNNI2), belongs to the troponin I gene family, and a part of the troponin complex including troponin T, troponin C and troponin I subunits. The troponin complex, along with tropomyosin, is responsible for the calcium-dependent regulation of striated muscle contraction. TNNI2 is also suppresses tumor growth in human ovarian carcinoma. Mutations in TNNI2 cause myopathy and distal arthrogryposis type 2B.

SNRPC is a member of the U1 small nuclear ribonucleoprotein C family. The SNRPC protein component of the U1 small nuclear ribonucleoprotein (snRNP) particle required for the formation of the spliceosome. SNRPC participates in the processing of nuclear precursor messenger RNA splicing. snRNP particles are tackled by autoantibodies frequently produced by patients with connective tissue diseases.

Major Histocompatibility Complex Class II DO Alpha (HLA-DOA) is a significant modulator in the HLA class II restricted antigen presentation pathway by interaction with the HLA-DM molecule in B-cells. HLA-DOA forms a heterodimer along with HLA-DOB. The heterodimer is located in lysosomes in B cells and regulates HLA-DM-mediated peptide loading on MHC class II molecules. HLA-DOA exhibits very little sequence variation, particularly at the protein level.

A 16-kDa peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores.

Geminin is a 25 kDa nuclear protein, which inhibits DNA replication and is degraded during the mitotic phase of the cell cycle. Geminin controls replication by binding to the licensing factor Cdt1, and is involved in neural differentiation. In addition, Geminin directly interacts with Six3 and Hox homeodomain proteins during embryogenesis and inhibits their functions. Geminin can also promote DNA replication. Geminin has 2 roles in 2 different stages of the cell cycle: Geminin is a negative regulator of DNA replication during the “S phase” of the cell cycle. Inhibition of Geminin during the “S phase” (by RNAi) results in an additional round of replication of portions of the genome. During the “M phase” of the cell cycle (mitosis) Geminin stabilizes the replication factor Cdt1 promoting DNA replication during the next cell cycle. Moreover, inhibition of Geminin during mitosis (by RNAi) causes destabilization of Cdt1 protein and impairment of DNA replication during the next cell cycle. Geminin thus guarantees that only one round of replication occurs during each cell cycle. It was discovered that Geminin is overexpressed in a number of malignancies and cancer cell lines. This maintains the concept that Geminin has also a positive role in DNA replication and cell cycle progression. Geminin accumulates through S, G2 and M phases of the cell cycle but is absent during the G1 phase. During the metaphase/anaphase transition of mitosis Geminin levels decrease.

ADAM12 is part of the A Disintegrin and Metalloprotease protein family wjich are membrane-anchored proteins structurally related to snake venom disintegrins, and are involved in a range of biological processes concerning cell-cell and cell-matrix interactions, including fertilization, muscle development, and eurogenesis.
ADAM12 has 2 alternatively spliced transcripts, a shorter/soluble secreted form called S-isoform and a longer membrane-bound form call L isoform. The S isoform is found to stimulate myogenesis. The short & soluble isoform lacks the transmembrane and cytoplasmic domains. ADAM12 S Isoform expression is limited to the placenta, embryo and foetus although levels have been detected in some tumour cell lines. ADAM12 takes part in skeletal muscle regeneration, specifically at the onset of cell fusion. ADAM12 is involved in macrophage-derived giant cells (MGC) and osteoclast formation from mononuclear precursors (by similarity).

Cardiotrophin 1 (CT-1) is a 201 amino acid member of the interleukin-6 superfamily. It was identified by its ability to induce hypertrophic response in cardiac myocytes. CT-1 mRNA levels were found both in cardiac myocytes and in cardiac nonmyocytes. CT 1 was also detected in abundance in normal adult human lung and was expressed in both fetal and adult airway smooth muscle cells. CT 1 activates gp130 dependent signaling and stimulates the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway to transduce hypertrophic and cytoprotective signals in cardiac myocytes.
CT 1 has also a neurotrophic function. CTF1 deficiency causes increased motoneuron cell death in spinal cord and brainstem nuclei of mice during a period between embryonic day 14 and the first postnatal week. Moreover, CT-1 is a hepatocyte survival factor that efficiently reduces hepatocellular damage in animal models of acute liver injury. Cardiotrophin 1 expression is augmented after hypoxic stimulation and it can protect cardiac cells when added either prior to simulated ischaemia or at the time of reoxygenation following simulated ischaemia. Cardiotrophin 1 can induce expression of the protective heat shock proteins (hsps) in cardiac cells.
Cardiotrophin-1 increased ventricular expression of ANP, brain natriuretic peptide (BNP) and angiotensinogen mRNA.
Cardiophin 1 levels were significantly elevated in patients with heart failure, patients with dilatative cardiomyopathy, moderate/severe mitral regurgitation, stable and unstable angina and after acute myocardial infarction.