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|Tested species reactivity||Human|
|Published species reactivity||Human, Mouse|
|Host / Isotype||Mouse / IgG2a, kappa|
|Immunogen||Human recombinant full length Pds1 protein|
|Storage buffer||PBS, pH 7.4, with 0.2% BSA|
|Contains||0.09% sodium azide|
|Storage Conditions||4° C|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:100-200|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Western Blot (WB)||See 8 publications below|
MA5-12252 targets Pds1 in IHC (P) applications and shows reactivity with Human samples.
The MA5-12252 immunogen is human recombinant full length Pds1 protein.
Pds1 is an anaphase inhibitor and plays important role in DNA damage and spindle check point pathways. Pds1 inhibits sister chromatid separation by binding and inhibiting Esp1, cystein protease that causes cleavage of the cohesin Scc1 that binds the sister chromatids together. Pds1 is responsible for targeting of Esp1 to nucleus and its binding to the spindle. Degradation of Pds1 occurs shortly before anaphase, which liberates Esp1 and is a prerequisite for anaphase entry. Pds1 is targeted for degradation by ubiquitination mediated by cyclosome/anaphase-promoting complex (APC) functioning as a ubiquitin ligase. In response to DNA damage Chk1 phosphorylates Pds1 to stabilize it against the APC mediated destruction, hence preventing the entry of such a cell into anaphase.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Down-regulation of the PTTG1 proto-oncogene contributes to the melanoma suppressive effects of the cyclin-dependent kinase inhibitor PHA-848125.
MA5-12252 was used in western blot to study the role of PTTG1 proto-oncogene down-regulation in the mechanism by which a cyclin-dependent kinase inhibitor retards melanoma growth
|Caporali S,Alvino E,Levati L,Esposito AI,Ciomei M,Brasca MG,Del Bufalo D,Desideri M,Bonmassar E,Pfeffer U,D'Atri S||Biochemical pharmacology (84:598)||2012|
Heat shock protein inhibitors, 17-DMAG and KNK437, enhance arsenic trioxide-induced mitotic apoptosis.
MA5-12252 was used in western blot to investigate the effect of 17-DMAG and KNK437 on arsenic trioxide cytotoxicity
|Wu YC,Yen WY,Lee TC,Yih LH||Toxicology and applied pharmacology (236:231)||2009|
Mitotic arrest-associated apoptosis induced by sodium arsenite in A375 melanoma cells is BUBR1-dependent.
MA5-12252 was used in western blot to investigate the mechanism for the induction of A375 cell death by sodium arsenite
|McNeely SC,Taylor BF,States JC||Toxicology and applied pharmacology (231:61)||2008|
Securin induces genetic instability in colorectal cancer by inhibiting double-stranded DNA repair activity.
MA5-12252 was used in western blot to examine the role of securin in the pathogenesis of colorectal cancer
|Kim DS,Franklyn JA,Smith VE,Stratford AL,Pemberton HN,Warfield A,Watkinson JC,Ishmail T,Wakelam MJ,McCabe CJ||Carcinogenesis (28:749)||2007|
Securin and separase phosphorylation act redundantly to maintain sister chromatid cohesion in mammalian cells.
MA5-12252 was used in western blot to study the redundancy of securin and separase phosphorylation in maintaining sister chromatid cohesion in mammalian cells
|Huang X,Hatcher R,York JP,Zhang P||Molecular biology of the cell (16:4725)||2005|
DNA damage-induced mitotic catastrophe is mediated by the Chk1-dependent mitotic exit DNA damage checkpoint.
MA5-12252 was used in western blot to study the role of Chk1 in mediating DNA damage-induced mitotic catastrophe
|Huang X,Tran T,Zhang L,Hatcher R,Zhang P||Proceedings of the National Academy of Sciences of the United States of America (102:1065)||2005|
Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control.
MA5-12252 was used in western blot to study the mechanisms underlying the promotion of genomic instability by Rb pathway inactivation
|Hernando E,Nahlé Z,Juan G,Diaz-Rodriguez E,Alaminos M,Hemann M,Michel L,Mittal V,Gerald W,Benezra R,Lowe SW,Cordon-Cardo C||Nature (430:797)||2004|
Complete loss of the tumor suppressor MAD2 causes premature cyclin B degradation and mitotic failure in human somatic cells.
MA5-12252 was used in western blot to study the effect of tumor suppressor MAD2 loss on premature cyclin B degradation and mitotic failure in human somatic cells
|Michel L,Diaz-Rodriguez E,Narayan G,Hernando E,Murty VV,Benezra R||Proceedings of the National Academy of Sciences of the United States of America (101:4459)||2004|
insulin-like growth factor 2 (somatomedin A); insulin-like growth factor II; insulin-like growth factor type 2; preptin; putative insulin-like growth factor II associated protein; somatomedin A; somatomedin-A; T3M-11-derived growth factor
C11orf43; GRDF; IGF-II; IGF2; PP1446; PP9974