Disease relevance of STREPTOZOTOCIN

• Acute leukemia after alkylating-agent therapy of ovarian cancer [1].
• Plasma-cell dyscrasia after alkylating-agent therapy for Hodgkin's disease [2].
• We studied 25 patients with acute nonlymphocytic leukemia in second remission (20 patients) or third remission (5 patients) in whom autologous bone marrow transplantation was performed with use of marrow incubated ex vivo with the alkylating agent 4-hydroperoxycyclophosphamide [3].
• In this study we show that the PpsR repressor from Rhodobacter sphaeroides binds to DNA in a redox-dependent manner through the formation/breakage of an intramolecular disulfide bond [4].
• When Escherichia coli is chronically exposed to very low, nontoxic doses of a monofunctional alkylating agent (notably N-methyl-N'-nitro-nitrosoguanidine, MNNG), the adaptive DNA repair pathway is induced which enables the bacteria to resist the killing and mutagenic effects of further alkylation damage [5].

Psychiatry related information on STREPTOZOTOCIN

• Alzheimer's disease cells exhibit defective repair of alkylating agent-induced DNA damage [6].
• The ability of three serotonin-uptake blockers to reverse the performance deficit in learning induced by previous uncontrollable stress (learned-helplessness paradigm) was investigated in streptozocin-induced diabetic rats [7].
• Prolonged food deprivation (FD) and streptozocin-induced diabetes (STZ diabetes) in the rat result in abolition of GH secretory episodes [8].
• In the present study a murine mAb (5G12-4, Ab3) that bears the 16/6 Id and binds to DNA was produced and was found to bind rabbit anti-16/6 Id sera and murine anti-16/6 Id mAb similarly to the human mAb 16/6 Id (Ab1) [9].
• Motor activity was assayed by sequentially adsorbing either kinesin or dynein to acid-washed coverslips, treating with an alkylating agent or control solution, adding microtubules and ATP, and finally imaging and quantifying the binding and gliding of microtubules using video-enhanced differential interference contrast (VE-DIC) microscopy [10].

High impact information on STREPTOZOTOCIN

• ParB binds to DNA sequences adjacent to the origin of replication suggesting that this region of the genome is tethered to the poles of the cell at a specific time in the cell cycle [11].
• Chemotherapy combinations that include an alkylating agent and a platinum coordination complex have high response rates in women with advanced ovarian cancer [12].
• As DNA-PK binds to DNA ends and is activated by these structures, our findings provide novel insights into V(D)J recombination and DNA repair processes [13].
• Fos and Jun, the protein products of the nuclear proto-oncogenes c-fos and c-jun, associate preferentially to form a heterodimer that binds to DNA and modulates transcription of a wide variety of genes in response to mitogenic stimuli [14].
• Thus, E47 binds to DNA both as a heterodimer with MyoD and as a homodimer, while E12 and MyoD bind to DNA efficiently only as heterodimers [15].

Chemical compound and disease context of STREPTOZOTOCIN

• The alkylating agent ifosfamide, an analog of cyclophosphamide, has demonstrated significant activity in soft tissue sarcoma and testicular carcinoma [16].
• Therefore, the effect of streptozocin-induced diabetes mellitus and dietary myo-inositol supplementation on rat sciatic nerve sodium-potassium ATPase was studied [17].
• Enhancement of alkylating agent activity by SR-4233 in the FSaIIC murine fibrosarcoma [18].
• The chemotherapeutic agent chlorozotocin, the 2-chloroethyl analogue of streptozocin, caused a decrease in plasma vasoactive intestinal polypeptide but caused significant renal toxicity with proteinuria [19].
• In a functional lactose permease mutant from Escherichia coli (LacY) devoid of native Cys residues, almost every residue was replaced individually with Cys and tested for reactivity with the permeant alkylating agent N-ethylmaleimide in right-side-out membrane vesicles [20].

Biological context of STREPTOZOTOCIN

• The S. cerevisiae RNA polymerase III (pol III) transcription factor TFIIIB binds to DNA upstream of the transcription start site of the SUP4 tRNA(Tyr) gene in a TFIIIC-dependent reaction and to the major 5S rRNA gene in a reaction requiring TFIIIC and TFIIIA [21].
• The erythroid-specific transcription factor Eryf1 binds to DNA sites within regulatory regions of every member of both the alpha- and beta-globin families in chicken [22].
• When cultures of Escherichia coli are exposed to a low level of the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) they accumulate mutations for about 20 min and then become resistant to further mutagenesis by that level of MNNG [23].
• Sac7d binds to DNA without any particular sequence preference and thereby increases its melting temperature by approximately 40 degrees C. We have now solved and refined the crystal structure of Sac7d in complex with two DNA sequences to high resolution [24].
• TFIIIA binds to DNA through its 30 K N-terminal domain, which contains nine zinc-fingers [25].

Anatomical context of STREPTOZOTOCIN

• We report here the identification of a human B-cell nuclear factor (IgNF-A) that binds to DNA sequences in the upstream regions of both the mouse heavy and kappa light-chain gene promoters and also to the mouse heavy-chain gene enhancer [26].
• Mice lacking the poly(ADP-ribose) polymerase gene are resistant to pancreatic beta-cell destruction and diabetes development induced by streptozocin [27].
• Because Ets2 is localized in the nucleus of macrophages and binds to DNA in vitro, the kinetics of its expression suggest a role for Ets2 in the transduction within the nucleus of specific signals received at the cell membrane and involved in securing the survival and/or the development of functional competence of these cells [28].
• Recombinant PEA3 binds to DNA with the same sequence specificity as that endogenous to FM3A cells and activates transcription through the PEA3 motif in HeLa cells [29].
• We also found that this phenomenon, which we refer to as "acquired multicellular resistance," is associated with an increase in intercellular adhesion or compaction of the alkylating agent-resistant cell lines grown as aggregates in three-dimensional culture [30].

Associations of STREPTOZOTOCIN with other chemical compounds

• We found that whereas p53 was induced by every genotoxic stimulus tested, c-Abl was activated by most stimuli except ultraviolet irradiation and JNK was strongly stimulated only by ultraviolet light and the alkylating agent methyl methanesulphonate [31].
• The alkylating agent cyclophosphamide may suppress or enhance immune responses in vivo but is inactive in vitro unless metabolized by microsomal enzyme activation [32].
• Islet transplantation under the kidney capsule fully corrects the impaired skeletal muscle glucose transport system of streptozocin diabetic rats [33].
• As previously described, there was an increase in insulin binding and a parallel increase in insulin-stimulated receptor phosphorylation in muscle of fasting and streptozotocin-induced (STZ) diabetic rats [34].
• ATPase activity was measured enzymatically in sciatic nerve homogenates from 4-wk streptozocin diabetic rats and age-matched controls either fed a standard or 1% myo-inositol supplemented diet [17].

Gene context of STREPTOZOTOCIN

• A derivative of GAL4 that binds to DNA but cannot activate transcription in yeast also fails to activate transcription in mammalian cells [35].
• NFAT and Osterix form a complex that binds to DNA, and this interaction is important for the transcriptional activity of Osterix [36].
• Drosophila Mad binds to DNA and directly mediates activation of vestigial by Decapentaplegic [37].
• We have shown that after a pulse of DNA damage in G1 with the alkylating agent MMS, there is also a MEC1-, RAD53-, and RAD9-dependent delay in G1 [38].
• RAP1 binds to DNA via two Myb/homeodomain-like motifs, which are DNA-binding folds previously identified in transcription factors [39].

Analytical, diagnostic and therapeutic context of STREPTOZOTOCIN

• After treatment with streptozocin (1.5 g per square meter) the plasma immunoreactive glucagon level decreased to 0.24 ng per milliliter [40].
• To determine whether this inability is due to inadequate insulin replacement, we studied fasted streptozocin-induced diabetic Lewis rats either untreated or after islet transplantation under the kidney capsule [33].
• Gel retardation assays demonstrated that the HD-Zip-1 domain binds to DNA as a dimer [41].
• Furthermore, DNA affinity chromatography of nucleoid extracts indicates that Mgm101p binds to DNA, suggesting that its nucleoid localization is in part due to this activity [42].
• As pretreatment, dimethyl myleran (DMM), an alkylating agent that produces effective myeloablation but little immunosuppression, was used with total body irradiation (TBI) [43].

References