KIAA0101, also known as p15(PAF), is a proliferating cell nuclear antigen-associated factor which interacts with proliferating cell nuclear antigen(PCNA). It was initially isolated in a yeast two-hybrid screen for PCNA binding partners, and was shown to bind PCNA competitively with the cell cycle regulator p21(WAF). KIAA0101 is localized primarily in the nucleus. It shares the conserved PCNA binding motif with several other PCNA binding proteins including CDK inhibitor p21 . KIAA0101 is involved in cell proliferation and plays a role in early tumor recurrence (ETR), and prognosis of hepatocellular carcinoma (HCC). KIAA0101 is expressed predominantly in liver, pancreas and placenta. It cannot be detected in heart or brain. It is highly expressed in a number of tumors, especially esophageal tumors, in anaplastic thyroid carcinomas and in non-small-cell lung cancer lines. Overexpression of KIAA0101 predicts high stage, early tumor recurrence, and poor prognosis of hepatocellular carcinoma. It also may be involved in protection of cells from UV-induced cell death.
KIFBP (Kinesin Family Binding Protein, also known as KIAA1279 and KIF1BP) is a Protein Coding gene. This gene encodes a kinesin family member 1 binding protein that is characterized by two tetratricopeptide repeats. The encoded protein localizes to the mitochondria and may be involved in regulating the transport of the mitochondria. Homozygous nonsense mutations in KIAA1279 at 1q22.1, encoding a protein with two tetratricopeptide repeats, underlie this syndromic form of Hirschsprung disease and generalized polymicrogyria, establishing the importance of KIAA1279 in both enteric and central nervous system development. KIAA1279 is widely expressed in the brain, testis, and other tissues. Diseases associated with KIFBP include Goldberg-Shprintzen Syndrome and Shprintzen-Goldberg Craniosynostosis Syndrome.
Kidney injury molecule-1 (KIM-1) (also known as TIM-1 and HAVCR) is a type 1 transmembrane glycoprotein found on activated CD4+ T cells, especially Th2 cells, and dedifferentiated proximal tubule epithelial cells. In humans, KIM-1 levels are very low or undetectable in normal samples, but following drug toxicity or ischemic damage to the kidney, the 85 kD, mucin-rich extracellular region of this molecule is shed and detected at elevated levels in urine, serum, and plasma. Therefore, KIM-1 is a suitable renal biomarker capable of early detection and progressive monitoring of acute kidney injury beyond traditional injury markers such as serum creatinine (SCr) and blood urea nitrogen (BUN) which lack specificity and sensitivity. KIM-1 has also been implicated in the development of atopic airway disease (asthma) and Th2-biased autoimmune responses.
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulinmucin 1 (TIM-1), is a type â,&hellip, , integral membrane glycoprotein. KIM-1 protein is widely expressed with highest levels in kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
Kininogen-1, also known as high molecular weight kininogen, williams-Fitzgerald-Flaujeac factor, Alpha-2-thiol proteinase inhibitor, Fitzgerald factor, KNG1 and BDK, is a secreted protein which contains threecystatin domains. Kininogen-1 / KNG1 is a protein from the blood coagulation system as well as the kinin-kallikrein system. It is a protein that adsorbs to the surface of biomaterials that come in contact with blood. Kininogen-1 / KNG1 circulates throughout the blood and quickly adsorbs to the material surfaces. Kininogen-1 / KNG1 is one of the early participants of the intrinsic pathway of coagulation, together with Factor XII (Hageman factor) and prekallikrein. Kininogen-1 / KNG1 is one of thekininogens, a class of proteins. As with many other coagulation proteins, the protein was initially named after the patients in whom deficiency was first observed. When the clinical data were combined, it turned out that all patients, in fact, had a deficiency of the same protein. Defects in KNG1 are the cause of high molecular weight kininogen deficiency (HMWK deficiency) which is an autosomal recessive coagulation defect. Patients with HWMK deficiency do not have a hemorrhagic tendency, but they exhibit abnormal surface-mediated activation of fibrinolysis.
Kininogen-1 is a secreted protein which contains three cystatin domains. There are two alternatively spliced forms, designated as the high molecular weight (HMW) and low MW (LMW) forms. Kininogen-1 plays a critical role in blood coagulation and inflammatory response. Kininogens are inhibitors of thiol proteases. Kininogen-1 participates in blood coagulation by helping to position optimally prekallikrein and factor XI next to factor XII, also inhibits the thrombin- and plasmin-induced aggregation of thrombocytes. The active peptide bradykinin that is released from Kininogen-1 shows a variety of physiological effects: influence in smooth muscle contraction, induction of hypotension, natriuresis and diuresis, decrease in blood glucose level. It is a mediator of inflammation and causes increase in vascular permeability, stimulation of nociceptors release of other mediators of inflammation. It has a cardioprotective effect. LMW-kininogen inhibits the aggregation of thrombocytes and doesn’t involved in blood clotting.
Killer cell immunoglobulin-like receptor 2DL1 or KIR2DL1 is an inhibitory natural Killer cell immunoglobulin-like receptor with two extracellular immunoglobulin domains. KIR2DL1 is a member of the Killer cell immunoglobulin-like receptor family whose members are classified by the number of the extracellular immunoglobulin domains and the length of the cytoplasm domain. KIR2DL1 is a transmembrane glycoprotein expressed by natural killer cells and subsets of T cells. KIR2DL1 down-regulates the cytotoxicity of NK cells upon recognition of specific class I major histocompatibility complex (MHC) molecules on target cells. It has been reported that the KIR2DL1 bound to its class I MHC ligand; HLA-Cw4. The KIR2DL1-HLA-Cw4 interface exhibits charge and shape complementarity. Specificity is mediated by a pocket in KIR2DL1 that hosts the Lys80 residue of HLA-Cw4. Many residues conserved in HLA-C and in KIR2DL receptors make different interactions in KIR2DL1-HLA-Cw4 and in a previously reported KIR2DL2-HLA-Cw3 complex. A dimeric aggregate of KIR-HLA-C complexes was observed in one KIR2DL1-HLA-Cw4 crystal.
Killer cell immunoglobulin-like receptor 2DL1 or KIR2DL1 is an inhibitory natural Killer cell immunoglobulin-like receptor with two extracellular immunoglobulin domains. KIR2DL1 is a member of the Killer cell immunoglobulin-like receptor family whose members are classified by the number of the extracellular immunoglobulin domains and the length of the cytoplasm domain. KIR2DL1 is a transmembrane glycoprotein expressed by natural killer cells and subsets of T cells. KIR2DL1 down-regulates the cytotoxicity of NK cells upon recognition of specific class I major histocompatibility complex (MHC) molecules on target cells. It has been reported that the KIR2DL1 bound to its class I MHC ligand, HLA-Cw4. The KIR2DL1-HLA-Cw4 interface exhibits charge and shape complementarity. Specificity is mediated by a pocket in KIR2DL1 that hosts the Lys80 residue of HLA-Cw4. Many residues conserved in HLA-C and in KIR2DL receptors make different interactions in KIR2DL1-HLA-Cw4 and in a previously reported KIR2DL2-HLA-Cw3 complex. A dimeric aggregate of KIR-HLA-C complexes was observed in one KIR2DL1-HLA-Cw4 crystal.
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