19553 Results for: "Sodium+carbonate+decahydrate"

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Key regulator of entry into cell division that acts as a tumor suppressor. Acts as a transcription repressor of E2F1 target genes. The underphosphorylated, active form of RB1 interacts with E2F1 and represses its transcription activity, leading to cell cycle arrest. Directly involved in heterochromatin formation by maintaining overall chromatin structure and, in particular, that of constitutive heterochromatin by stabilizing histone methylation. Recruits and targets histone methyltransferases SUV39H1, SUV420H1 and SUV420H2, leading to epigenetic transcriptional repression. Controls histone H4 'Lys-20' trimethylation. Inhibits the intrinsic kinase activity of TAF1. In case of viral infections, interactions with SV40 large T antigen, HPV E7 protein or adenovirus E1A protein induce the disassembly of RB1-E2F1 complex thereby disrupting RB1's activity.

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Key regulator of entry into cell division that acts as a tumor suppressor. Acts as a transcription repressor of E2F1 target genes. The underphosphorylated, active form of RB1 interacts with E2F1 and represses its transcription activity, leading to cell cycle arrest. Directly involved in heterochromatin formation by maintaining overall chromatin structure and, in particular, that of constitutive heterochromatin by stabilizing histone methylation. Recruits and targets histone methyltransferases SUV39H1, SUV420H1 and SUV420H2, leading to epigenetic transcriptional repression. Controls histone H4 'Lys-20' trimethylation. Inhibits the intrinsic kinase activity of TAF1. In case of viral infections, interactions with SV40 large T antigen, HPV E7 protein or adenovirus E1A protein induce the disassembly of RB1-E2F1 complex thereby disrupting RB1's activity.

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General protein kinase capable of phosphorylating several known proteins. Phosphorylates TBC1D4. Signals downstream of phosphatidylinositol 3-kinase (PI3K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Plays a role in glucose transport by mediating insulin-induced translocation of the GLUT4 glucose transporter to the cell surface. Mediates the antiapoptotic effects of IGF-I. Mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1. Promotes glycogen synthesis by mediating the insulin-induced activation of glycogen synthase.

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Motor brushes for centrifuge 1 * 2 items

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Key regulator of entry into cell division that acts as a tumor suppressor. Acts as a transcription repressor of E2F1 target genes. The underphosphorylated, active form of RB1 interacts with E2F1 and represses its transcription activity, leading to cell cycle arrest. Directly involved in heterochromatin formation by maintaining overall chromatin structure and, in particular, that of constitutive heterochromatin by stabilizing histone methylation. Recruits and targets histone methyltransferases SUV39H1, SUV420H1 and SUV420H2, leading to epigenetic transcriptional repression. Controls histone H4 'Lys-20' trimethylation. Inhibits the intrinsic kinase activity of TAF1. In case of viral infections, interactions with SV40 large T antigen, HPV E7 protein or adenovirus E1A protein induce the disassembly of RB1-E2F1 complex thereby disrupting RB1's activity.

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Involved in chromosome cohesion during cell cycle and in DNA repair. Central component of cohesin complex. The cohesin complex is required for the cohesion of sister chromatids after DNA replication. The cohesin complex apparently forms a large proteinaceous ring within which sister chromatids can be trapped. At anaphase, the complex is cleaved and dissociates from chromatin, allowing sister chromatids to segregate. The cohesin complex may also play a role in spindle pole assembly during mitosis. Involved in DNA repair via its interaction with BRCA1 and its related phosphorylation by ATM, or via its phosphorylation by ATR. Works as a downstream effector both in the ATM/NBS1 branch and in the ATR/MSH2 branch of S-phase checkpoint.

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NF-κ-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-κ-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively.

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FES (feline sarcoma oncogene) and Fer are the only two members of a unique family of cytoplasmic protein tyrosine kinases.FES and Fer contain a central Src homology-2 (SH2) domain and a carboxy-terminal tyrosine kinase catalytic domain. They are structurally distinguished from other members of cytoplasmic protein tyrosine kinase subfamilies by the presence of amino-terminal Fer/CIP4 homology and coiled-coil domains. FES was originally identified as an oncogene from avian and feline retroviruses. Human c-Fes has been implicated in myeloid, vascular endothelial and neuronal cell differentiation. FES has tyrosine-specific protein kinase activity and that activity is required for maintenance of cellular transformation. Mutations may activate the FES kinase and thereby contribute to cancer. However, recent data strongly suggests that the c-FES protein-tyrosine kinase is a tumor suppressor rather than a dominant oncogene in colorectal cancer.

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Cyclin-dependent kinase activity is regulated by T-loop phosphorylation (Thr172 in the case of CDK4), by the abundance of their cyclin partners, and by association with CDK inhibitors of the Cip/Kip or INK family of proteins. The inactive ternary complex of CDK4/cyclin D and p27 Kip1/Cip1 requires extracellular mitogenic stimuli for the release and degradation of p27, which affects progression through the restriction point and pRb-dependent entry into S-phase. The active complex of CDK4/cyclin D targets the retinoblastoma protein for phosphorylation, allowing the release of E2F transcription factors that activate G1/S-phase gene expression. In HeLa cells, upon UV irradiation, upregulation of p16 INK4A association with CDK4/cyclin D3 leads to a G2 delay, implicating CDK4/cyclin D3 activity in progression through the G2-phase of the cell cycle.

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Heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) is a member of the hnRNP A/B family of related RNA binding proteins that bind pre-mRNA and are involved in the processing, metabolism and transport of nuclear pre-mRNA transcripts. hnRNP A1 regulates the alternative splicing of c-Src, c-H-Ras and modifies initiation of translation of the fibroblast growth factor 2 mRNA. hnRNP A1 expression level is elevated in many cancers; knockdown of hnRNP A1 leads to apoptosis in various cancer cells. Although predominantly nuclear, hnRNP A1 is continually transported from the nucleus to the cytoplasm where it disassociates from mRNA and is rapidly re-imported into the nucleus. hnRNP A1 binds to cis-acting repressive sequences (CRS) of HIV-1 to influence HIV-1 production. HIV-1 enhances hnRNP A1 expression and promotes the relocalization of hnRNP A1 to the cytoplasm ,

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Hsp90 is a member of the heat shock protein 90 family that functions as a molecular chaperone and has ATPase activity. Hsp90 family proteins are highly conserved between isoforms and species. Several signal transduction pathways depend on Hsp90 function including erbB2, steroid hormone receptors (such as androgen, progesterone, glucocorticoid, and aryl-hydrocarbon), and hypoxia sensing (Hif1alpha). Recent reports show that tumor cells are more sensitive to Hsp90 inhibition and that Hsp90 from tumor cells is more sensitive to small molecule inhibitors (eg 17AAG). The mechanism of this differential sensitivity of normal versus tumor Hsp90 is not known (although mutation has been ruled out). One possible mechanism may be differences in post-translational modification of tumor Hsp90. Hsp90 is a cytoplasmic protein that forms a homodimer in vivo, and interacts with TOM34, AHSA1, HDAC6 and SMYD3.

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S-Monovette® is a blood collection system that combines two blood collection techniques – aspiration and vacuum. The S-Monovette® is suitable for all vein conditions and achieves an optimal sample quality, thereby producing the best results. The aspiration technique is a gentle technique for routine blood collection. Using the vacuum technique, a "fresh" vacuum is always available.

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Alpha-tubulin belongs to the tubulin superfamily, which is composed of six distinct families. Along with beta-tubulins, alpha-tubulins are the major components of microtubules. These microtubules are involved in a wide variety of cellular activities ranging from mitosis and transport events to cell movement and the maintenance of cell shape. Alpha- and beta-tubulin dimers are assembled to 13 protofilaments that form a microtubule of 22-nm diameter (reviewed in 1). Tyrosine ligase adds a C-terminal tyrosine to monomeric alpha-tubulin. Assembled microtubules can again be detyrosinated by a cytoskeleton-associated carboxypeptidase (2). Another post-translational modification of detyrosinated alpha-tubulin is C-terminal polyglutamylation, which is characteristic of microtubules in neuronal cells and the mitotic spindle (3). Like GAPDH and beta-Actin, this antibody makes an excellent loading control in immunoblots.

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CCNT1 Antibody: Cyclins function as regulators of CDK kinases and exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. The cyclin-T1 protein (CCNT1) belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. CCNT1 tightly associates with CDK9 kinase, and was found to be a major subunit of the transcription elongation factor p-TEFb. The kinase complex containing CCNT1 and the elongation factor can interact with, and act as a cofactor of human immunodeficiency virus type 1 (HIV-1) Tat protein, and was shown to be both necessary and sufficient for full activation of viral transcription. CCNT1 and its kinase partner were also found to be involved in the phosphorylation and regulation of the carboxy-terminal domain (CTD) of the largest RNA polymerase II subunit.

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SkillPak 1 and 5 ml columns are designed for fast method development, resin screening or sample concentration. Pre-packed with TOYOPEARL®, TSKgel® or Ca++Pure-HA™ process chromatography media, these columns offer superior separation of biomelocules, such as monoclonal antibodies, proteins and oligonucleotides. SkillPak 50 and 200 ml pre-packed columns are the best solution for seamless scale up of methods developed on SkillPak 1 and 5.

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This gene is a target gene of the transcription factor tumor protein p53. The encoded protein is a nuclear phosphoprotein that binds and inhibits transactivation by tumor protein p53, as part of an autoregulatory negative feedback loop. Overexpression of this gene can result in excessive inactivation of tumor protein p53, diminishing its tumor suppressor function. This protein has E3 ubiquitin ligase activity, which targets tumor protein p53 for proteasomal degradation. This protein also affects the cell cycle, apoptosis, and tumorigenesis through interactions with other proteins, including retinoblastoma 1 and ribosomal protein L5. More than 40 different alternatively spliced transcript variants have been isolated from both tumor and normal tissues

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IGF1R(insulin-like growth factor 1 receptor), a transmembrane receptor tyrosine kinase, is widely expressed in many cell types within fetal and postnatal tissues, and in many cell lines. Upon binding to its ligands, IGF-I and IGF-II, receptor autophosphorylation occurs. The triple tyrosine cluster within the kinase domain (Tyr1131, Tyr1135 and Tyr1136) is the earliest major site of autophosphorylation. Phosphorylation of these three tyrosine residues is necessary for kinase activation.Insulin receptors (IRs) share significant similarity with IGF1 receptors in both structure and function,including an equivalent triple tyrosine cluster within the activation loop of the kinase domain (Tyr1146, Tyr1150 and Tyr1151).Tyrosine autophosphorylation of insulin receptor is one of the earliest cellular responses to insulin stimulation. Autophosphorylation begins with phosphorylation of Tyr1146 and either Tyr1150 or Tyr1151. Full kinase activation requires the triple tyrosine phosphorylation.

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CD31, also known as platelet endothelial cell adhesion molecule 1 (PECAM1), is a type I integral membrane glycoprotein and a member of the immunoglobulin superfamily of cell surface receptors.It is constitutively expressed on the surface of endothelial cells, and concentrated at the junction between them. The antibody reacts with the murine form of the Platelet-Endothelial Cell Adhesion Molecule. The reactivity of the antibody is restricted to the isoform of the molecule that is selectively expressed by endothelial cells.The antigen is predominantly present at the lateral borders of endothelial cells as described for human PECAM-1.It is also weakly expressed on many peripheral lymphoid cells and platelets.CD31 has been used to measure angiogenesis in association with tumor recurrence. Other studies have also indicated that CD31 and CD34 can be used as markers for myeloid progenitor cells and recognize different subsets of myeloid leukemia infiltrates (granular sarcomas).

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PRAK (p38-regulated /activated kinase), also referred to as mitogen-activated protein kinase (MAPK)-activated protein kinase (MAPKAPK)-5, is an ubiquitously expressed serine/threonine kinase regulated by p38beta and p38beta MAP kinases. Activated JNK, p38gamma or p38δ are unable to induce phosphorylation of PRAK in vitro. Phosphorylation of PRAK occurs in vivo in response to p38 activation by stress-related extracellular stimuli including UV light, oxidation and proinflammatory cytokines. Two other substrates for p38, MAPKAPK-2 and MAPKAPK-3/3pK, share approximately 45% sequence homology with PRAK including the phosphorylation motif recognized by p38, Lys-X-Thr-Pro. Activated PRAK has been shown to specifically phosphorylate HSP 27 in vitro, suggesting that the protein may play a role in stress-induced small heat shock protein phosphorylation in vivo.

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Ligand for the receptor-type protein-tyrosine kinase KIT. Plays an essential role in the regulation of cell survival and proliferation, hematopoiesis, stem cell maintenance, gametogenesis, mast cell development, migration and function, and in melanogenesis. KITLG/SCF binding can activate several signaling pathways. Promotes phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, and subsequent activation of the kinase AKT1. KITLG/SCF and KIT also transmit signals via GRB2 and activation of RAS, RAF1 and the MAP kinases MAPK1/ERK2 and/or MAPK3/ERK1. KITLG/SCF and KIT promote activation of STAT family members STAT1, STAT3 and STAT5. KITLG/SCF and KIT promote activation of PLCG1, leading to the production of the cellular signaling molecules diacylglycerol and inositol-1, 4, 5-trisphosphate. KITLG/SCF acts synergistically with other cytokines, probably interleukins.

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Alpha-tubulin Antibody: Alpha-tubulin belongs to the tubulin superfamily, which is composed of six distinct families. Along with beta-tubulins, alpha-tubulins are the major components of microtubules. These microtubules are involved in a wide variety of cellular activities ranging from mitosis and transport events to cell movement and the maintenance of cell shape. Alpha- and beta-tubulin dimers are assembled to 13 protofilaments that form a microtubule of 22-nm diameter. Tyrosine ligase adds a C-terminal tyrosine to monomeric alpha-tubulin. Assembled microtubules can again be detyrosinated by a cytoskeleton-associated carboxypeptidase. Another post-translational modification of detyrosinated alpha-tubulin is C-terminal polyglutamylation, which is characteristic of microtubules in neuronal cells and the mitotic spindle. Like GAPDH and beta-Actin, this antibody makes an excellent loading control in immunoblots.

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Lin28 Monoclonal Antibody: Lin28 is a transcription factor that was first identified through its key role in the pathway of developmental timing in C. elegans. The role of Lin28 in development suggested that it might be useful in the creation of stem cells that might be beneficial in cell replacement therapies in the treatment of several degenerative diseases. Artificial stem cells, termed induced pluripotent stem (iPS) cells, can be created by expressing Lin28 in addition to the transcription factors POU5F1, Sox2, and NANOG in mouse fibroblasts. More recently, experiments have demonstrated that iPS cells could be generated using expression plasmids expressing Lin28, Sox2, POU5F1 and c-Myc, eliminating the need for virus introduction, thereby addressing a safety concern for potential use of iPS cells in regenerative medicine.

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FILTER GENERAL PURPOSE ORGANIC SOL B-100 1 * 1 items

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CCL4 Antibody: CCL4, also known as macrophage inflammatory protein 1-beta (MIP1B), belongs to the intercrine beta (chemokine CC) family. Both CCL4 and the related protein CCL3 participate in the host response to invading bacterial, viral, parasite and fungal pathogens by regulating the trafficking and activation state of selected subgroups of inflammatory cells. While both CCL4 and CCL3 exert similar effects on monocytes, their effect on lymphocytes differ; with CCL4 selectively attracting CD4+ lymphocytes and CCL3 selectively attracting CD8+ lymphocytes. Additionally, both have been shown to be potent chemoattractants for B cells, eosinophils and dendritic cells. The processed form of CCL4 can induce down-modulation of surface expression of the chemokine receptor CCR5, thus inhibiting the CCR5-mediated entry of HIV-1 in T cells.

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Key regulator of entry into cell division that acts as a tumor suppressor. Acts as a transcription repressor of E2F1 target genes. The underphosphorylated, active form of RB1 interacts with E2F1 and represses its transcription activity, leading to cell cycle arrest. Directly involved in heterochromatin formation by maintaining overall chromatin structure and, in particular, that of constitutive heterochromatin by stabilizing histone methylation. Recruits and targets histone methyltransferases SUV39H1, SUV420H1 and SUV420H2, leading to epigenetic transcriptional repression. Controls histone H4 'Lys-20' trimethylation. Inhibits the intrinsic kinase activity of TAF1. In case of viral infections, interactions with SV40 large T antigen, HPV E7 protein or adenovirus E1A protein induce the disassembly of RB1-E2F1 complex thereby disrupting RB1's activity.

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General protein kinase capable of phosphorylating several known proteins. Phosphorylates TBC1D4. Signals downstream of phosphatidylinositol 3-kinase (PI3K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). Plays a role in glucose transport by mediating insulin-induced translocation of the GLUT4 glucose transporter to the cell surface. Mediates the antiapoptotic effects of IGF-I. Mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1. Promotes glycogen synthesis by mediating the insulin-induced activation of glycogen synthase.

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ITGA4 encodes integrin alpha chain 4. Integrins are heterodimeric integral membrane proteins composed of an alpha chain and a beta chain. Unlike other integrin alpha chains, alpha 4 neither contains an I-domain, nor undergoes disulfide-linked cleavage. Although alpha 4 is variably cleaved to yield two unlinked chains, this cleavage is unnecessary for integrin assembly and function. Alpha 4 combines with beta 1 (ITGB1) on T-cells to form the integrin very late (activation) antigen 4 (VLA-4) that can bind to the extracellular matrix molecules fibronectin or thrombospondin, and is also a ligand for the cell surface molecule vascular cell adhesion molecule 1 (VCAM-1). In addition, alpha 4 combines with beta 7 to form the lymphocyte homing receptor known as LPAM-1 (lymphocyte Peyer Patch adhesion molecule 1). Integrins are also known to participate in cell-surface mediated signalling.

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Integrin alpha-V/beta-3 is a receptor for cytotactin, fibronectin, laminin, matrix metalloproteinase-2, osteopontin, osteomodulin, prothrombin, thrombospondin, vitronectin and von Willebrand factor. Integrin alpha-IIb/beta-3 is a receptor for fibronectin, fibrinogen, plasminogen, prothrombin, thrombospondin and vitronectin. Integrins alpha-IIb/beta-3 and alpha-V/beta-3 recognize the sequence R-G-D in a wide array of ligands. Integrin alpha-IIb/beta-3 recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain. Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen. This step leads to rapid platelet aggregation which physically plugs ruptured endothelial surface. In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions.

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Transcriptional coactivator which acts as a downstream regulatory target in the Hippo signaling pathway that plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis. The core of this pathway is composed of a kinase cascade wherein MST1/MST2, in complex with its regulatory protein SAV1, phosphorylates and activates LATS1/2 in complex with its regulatory protein MOB1, which in turn phosphorylates and inactivates YAP1 oncoprotein and WWTR1/TAZ. WWTR1 enhances PAX8 and NKX2-1/TTF1-dependent gene activation. Regulates the nuclear accumulation of SMADS and has a key role in coupling them to the transcriptional machinery such as the mediator complex. Regulates embryonic stem-cell self-renewal, promotes cell proliferation and epithelial-mesenchymal transition.

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ALAS-1 (EC 2.3.1.37) is a nuclear-encoded mitochondrial matrix enzymecatalyzing the condensation of glycine with succinyl-CoA to form delta-amino levulinate, CO2 and CoA. It regulates the first and rate-limiting step of heme biosynthetic pathway. It is one of the two isoforms of ALAS and is a pyridoxal-5 phosphate dependant housekeeping enzyme. It is ubiquitously expressed and is responsible of providing heme for cytochromes and other hemoproteins. ALAS1 in liver undergoes negative feedback regulation by heme. Transcription of ALAS1 gene is stimulated by cAMP and respiratory uncoupling whereas Phorbol esters and insulin repress ALAS1 gene expression. ALAS1 is suggested to be involved in reciprocal regulation of Heme biosynthesis and circadian clock suggesting a potential target for treatment of circadian disorders. ALAS1 gene expression is down regulated in Acute Liver failure resulting in altered heme metabolism and liver function.