- 34-6300 - Invitrogen Antibodies CDKN1B antibody

Submitted references MARCKS Signaling Differentially Regulates Vascular Smooth Muscle and Endothelial Cell Proliferation through a KIS-, p27kip1- Dependent Mechanism.

Yu D, Makkar G, Dong T, Strickland DK, Sarkar R, Monahan TS
PloS one 2015;10(11):e0141397

Cdk5 and its substrates, Dcx and p27kip1, regulate cytoplasmic dilation formation and nuclear elongation in migrating neurons.

Nishimura YV, Shikanai M, Hoshino M, Ohshima T, Nabeshima Y, Mizutani K, Nagata K, Nakajima K, Kawauchi T
Development (Cambridge, England) 2014 Sep;141(18):3540-50

Expression of CRM1 in human gliomas and its significance in p27 expression and clinical prognosis.

Shen A, Wang Y, Zhao Y, Zou L, Sun L, Cheng C
Neurosurgery 2009 Jul;65(1):153-9; discussion 159-60

Expression of Jun activation domain-binding protein 1 and Ser10 phosphorylated p27 protein in human epithelial ovarian carcinoma.

Wang Y, Wang Y, Cheng C, Ji Y, Zhao Y, Zou L, Shen A
Journal of cancer research and clinical oncology 2009 Jul;135(7):951-9

Jun activation domain-binding protein 1 negatively regulate p27 kip1 in non-Hodgkin's lymphomas.

Wang Y, Fei M, Cheng C, Zhang D, Lu J, He S, Zhao Y, Wang Y, Shen A
Cancer biology & therapy 2008 Mar;7(3):460-7

Jun activation domain-binding protein 1 negatively regulate p27 kip1 in non-Hodgkin's lymphomas.

Wang Y, Fei M, Cheng C, Zhang D, Lu J, He S, Zhao Y, Wang Y, Shen A
Cancer biology & therapy 2008 Mar;7(3):460-7

Differential modification of p27Kip1 controls its cyclin D-cdk4 inhibitory activity.

James MK, Ray A, Leznova D, Blain SW
Molecular and cellular biology 2008 Jan;28(1):498-510

Endothelin is a dose-dependent trophic factor and a mitogen in small arteries in vivo.

Dao HH, Bouvet C, Moreau S, Beaucage P, Larivière R, Servant MJ, de Champlain J, Moreau P
Cardiovascular research 2006 Jul 1;71(1):61-8

Shp-1 mediates the antiproliferative activity of tissue inhibitor of metalloproteinase-2 in human microvascular endothelial cells.

Seo DW, Li H, Qu CK, Oh J, Kim YS, Diaz T, Wei B, Han JW, Stetler-Stevenson WG
The Journal of biological chemistry 2006 Feb 10;281(6):3711-21

Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice.

Uchida T, Nakamura T, Hashimoto N, Matsuda T, Kotani K, Sakaue H, Kido Y, Hayashi Y, Nakayama KI, White MF, Kasuga M
Nature medicine 2005 Feb;11(2):175-82

The cyclin-dependent kinase inhibitor p27Kip1 is stabilized in G(0) by Mirk/dyrk1B kinase.

Deng X, Mercer SE, Shah S, Ewton DZ, Friedman E
The Journal of biological chemistry 2004 May 21;279(21):22498-504

The role of cyclin-dependent kinase inhibitor p27Kip1 in anti-HER2 antibody-induced G1 cell cycle arrest and tumor growth inhibition.

Le XF, Claret FX, Lammayot A, Tian L, Deshpande D, LaPushin R, Tari AM, Bast RC Jr
The Journal of biological chemistry 2003 Jun 27;278(26):23441-50

No comments: Submit comment

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of recombinant purified wild-type p27 and p27 (S10A) mutants after phosphorylation in vivo by either cyclin E-Cdk2 (lanes 1 and 2) or ERK2 (lanes 3 and 4) using Rb anti-phospho-p27 (Ser10) (Product # 34-6300) (top), Rb anti-phospho-p27 (Thr187) (Product # 71-7700) (middle), and a monoclonal antibody to p27 (bottom). Image reproduced from Rodier G, et al. EMBO J 2001.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 6 MARCKS knockdown increases KIS expression and cell proliferation in endothelial cells. A. Human coronary artery ECs were treated with 20 nM non-targeting, control or MARCKS siRNA. Four days after transfection, MARCKS knockdown increased both KIS and pSer10-p27 kip1 protein expression. B. Endothelial cells were cultured at subconfluence and they remained subconfluent for the duration of the experiment. MARCKS knockdown also resulted in 25+-6% ( p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 3 MARCKS knockdown decreases p27 kip1 , pSer10-p27 kip1 , KIS, cyclin D1, and ubiquitin ligase E3 Skp2, but does not affect cyclin E1 protein expression. A. The cyclin-dependent kinase inhibitor p27 kip1 protein expression is regulated in a multistep process by degradation by the 26s proteasome. B. Human coronary artery smooth muscle cells (CASMCs) were treated with MARCKS siRNA or non-targeting siRNA (Control). Protein expression was determined by Western Blot analysis. C. Protein expression was normalized to beta-actin and compared with densitometry. Expression of pSer10-p27 kip1 , pThr187-p27 kip1 , KIS, cyclin D1, and the E3 ubiquitin protein ligase all decreased significantly with MARCKS knockdown. Only Cylcin E did not change significantly as a result of MARCKS knockdown. KIS and pSer10-p27 kip1 had the greatest decrease in protein expression as a result of MARCKS knockdown. All experiments were performed in triplicate. Statistical significance was determined by the two-tailed Student's t -test. * denotes p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 5 MARCKS knockdown induced p27 kip1 nuclear trapping is released by co-transfection with wild-type kinase interacting with stathmin (KIS). A. Rat aortic vascular smooth muscle A7r5 cells were transfected with either non-targeting, control siRNA or MARCKS siRNA and co-transfected with DNA plasmids expressing wild-type KIS (WT KIS), or kinase-dead mutant KIS (K54R KIS). MARCKS siRNA knockdown and expression of KIS plasmids were confirmed by Western blot analysis. B. Co-transfection with wild-type KIS released the nuclear trapping of p27 kip1 (white arrows) in MARCKS knockdown cells, but kinase-dead KIS (K45R KIS) did not. C. A total of 150 cells were scored in each treatment allowing for quantitative analysis (white arrows in Fig 5B indicate examples of cells counted as with phenotype of p27 kip1 nuclear accumulation). Nuclear trapping of p27 kip1 after MARCKS knockdown was released by co-transfection with wild-type KIS but not kinase dead KIS (K45R). Scale bar = 10 mum, * denotes p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 1 Cell cycle analysis after siRNA-mediated MARCKS knockdown in vascular smooth muscle cells. A. Cell cycle progression of human coronary artery smooth muscle cells (CASMCs) was determined by FACS analysis after treated with either 80 nM control, non-targeting siRNA, or MARCKS siRNA. MARCKS knockdown resulted in a significantly greater proportion of cells in phase G 0 /G 1 compared to cells treated with control non-targeting siRNA, 78% compared to 55% respectively. MARCKS knockdown also resulted in fewer cells in phase G2/M than control, 17% and 40% respectively (Chi 2 statistic 13.3, p

34-6300

Antibody data