MA5-13338

antibody from Invitrogen Antibodies

Targeting: CDK6 PLSTIRE

Western blot (Supportive data in Antibodypedia)

Immunoprecipitation (Data presented on provider website)

Immunohistochemistry (Recommended by provider)

Other assay (Supportive data in Antibodypedia)

Antibody Data

Product number

MA5-13338

Provider

Invitrogen Antibodies

Product name

CDK6 Monoclonal Antibody (K6.90 (DCS-90))

Antibody type

Monoclonal

Antigen

Purifed from natural sources

Description

MA5-13338 targets Cdk6 in IF, IHC (F), IP, and WB applications and shows reactivity with Human, mouse, and Rat samples. The MA5-13338 immunogen is purified recombinant cdk6 protein.

Reactivity

Human, Mouse, Rat

Host

Mouse

Isotype

IgG

Antibody clone number

K6.90 (DCS-90)

Vial size

500 µL

Concentration

0.2 mg/mL

Storage

4° C

References

Submitted references

Suppressing STAT5 signaling affects osteosarcoma growth and stemness.

Subramaniam D, Angulo P, Ponnurangam S, Dandawate P, Ramamoorthy P, Srinivasan P, Iwakuma T, Weir SJ, Chastain K, Anant S
Cell death & disease 2020 Feb 24;11(2):149

---

MiR-34a chemosensitizes bladder cancer cells to cisplatin treatment regardless of p53-Rb pathway status.

Vinall RL, Ripoll AZ, Wang S, Pan CX, deVere White RW
International journal of cancer 2012 Jun 1;130(11):2526-38

---

p16INK4a-induced senescence is disabled by melanoma-associated mutations.

Haferkamp S, Becker TM, Scurr LL, Kefford RF, Rizos H
Aging cell 2008 Oct;7(5):733-45

---

p16INK4a-induced senescence is disabled by melanoma-associated mutations.

Haferkamp S, Becker TM, Scurr LL, Kefford RF, Rizos H
Aging cell 2008 Oct;7(5):733-45

---

Cyclin D2 and cyclin D3 play opposite roles in mouse skin carcinogenesis.

Rojas P, Cadenas MB, Lin PC, Benavides F, Conti CJ, Rodriguez-Puebla ML
Oncogene 2007 Mar 15;26(12):1723-30

Western blot

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

A549 cells were lysed 72 hours after transfection. Cells were transfected with Transfection Reagent alone (Lane 1), 100nM ON-TARGETplus siCONTROL Non-Targeting Pool (Lane 2), or 100nM ONTARGETplus CDK6 siRNA (Lane 3). Western blot data for CyclophilinB is included as a control for equal protein loading.

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Western blot of Cdk6 using Cdk6 Monoclonal Antibody (Product # MA5-13338) on LS174T Cells.

Other assay

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Immunoprecipitation of Cdk6 using Cdk6 Monoclonal Antibody (Product # MA5-13338) on Native Human LS174T Cells.

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Fig. 2 Pimozide induces cell cycle arrest and apoptosis. a Cell cycle analysis of pimozide treated cells. KHOS/NP and SJSA-1 were treated with 20 uM of pimozide for 24 and 48 h and then examined by flow cytometry following propidium iodide staining for DNA content. Pimozide treatment increased SubG0/G1 arrest at 24 and 48 h in both cells. b Cells were incubated with pimozide 10 and 20 uM concentration for 24 h and assessed for apoptosis by Caspase3/7 assay. Pimozide treatment results in significant increase in caspase-3/7 activity in both KHOS/NP and SJSA-1 cells (* p < 0.001). c Cells were treated with 20 muM of pimozide for 24 and 48 h, the lysate was analyzed by western blotting for Caspase 3 and PARP protein expression. Both the cell lines showed caspase 3 cleavage and PARP cleavage following pimozide treatment. d Lysates from cells incubated with 20 uM of pimozide were analyzed by western blotting for cyclin D1, along with CDK2 and phosphorylation of RB levels. Pimozide inhibits cyclin D1, CDK2 expressions and phosphorylation of RB levels in both KHOS/NP and SJSA-1 cells. e Cells wer e treated with 20 muM of pimozide for 24 and 48 h, the lysate was analyzed by western blotting for anti-apoptotic and pro-apoptotic proteins. Pimozide treatment resulted in decreased levels of Bcl2 and Bcl-XL expression and increased Bax expression in both KHOS/NP and SJSA-1 cells.