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Huntington's disease (HD), a neurodegenerative disorder characterized by loss of striatal neurons, is caused by an expansion of a polyglutamine tract in the HD protein huntingtin. Additionally we are shipping and many more products for this protein.
Showing 10 out of 72 products:
Dog (Canine) Polyclonal SETD2 Primary Antibody for IHC, WB - ABIN2783051
Barrand, Andersen, Collas: Promoter-exon relationship of H3 lysine 9, 27, 36 and 79 methylation on pluripotency-associated genes. in Biochemical and biophysical research communications 2010
Mouse (Murine) Polyclonal SETD2 Primary Antibody for ELISA, WB - ABIN262286
Sun, Wei, Wu, Hu, Wang, Wang, Zhang, Chen, Huang, Chen: Identification and characterization of a novel human histone H3 lysine 36-specific methyltransferase. in The Journal of biological chemistry 2005
Human Polyclonal SETD2 Primary Antibody for ICC, IF - ABIN4320758
Kanu, Grönroos, Martinez, Burrell, Yi Goh, Bartkova, Maya-Mendoza, Mistrík, Rowan, Patel, Rabinowitz, East, Wilson, Santos, McGranahan, Gulati, Gerlinger, Birkbak, Joshi, Alexandrov, Stratton, Powles et al.: SETD2 loss-of-function promotes renal cancer branched evolution through replication stress and impaired DNA repair. ... in Oncogene 2015
Mutation in SETD2 gene is associated with renal cell carcinoma (show MOK Antibodies).
Data identify SETD2 as a dual-function methyltransferase for both chromatin and the cytoskeleton and show a requirement for methylation in maintenance of genomic stability and the integrity of both the tubulin (show TUBB Antibodies) and histone codes.
This study provides evidence for HOTAIR to promote tumorigenesis via downregulating SETD2 in liver cancer stem cells.
Use bioinformatic tools to predict the molecular effects of all mutations lying in SETD2 genes.
This study provide the evidence SETD2 mutation releate to Autism Spectrum Disorder.
Data show that SETD2 mutations are not associated with microsatellite instability in renal cancer and suggest a role for SETD2 in maintaining genome integrity through nucleosome stabilization, DNA repair and suppression of replication stress.
Findings extend the knowledge about the regulation of SETD2 at the posttranscriptional level by miRNA and regulatory mechanism downstream of SETD2 in ccRCC.
loss of SETD2 may afford an alternative mechanism for the inactivation of the p53 (show TP53 Antibodies)-mediated checkpoint without the need for additional genetic mutations in TP53 (show TP53 Antibodies).
Mutations in epigenetic regulators including SETD2 are gained during relapse in paediatric acute lymphoblastic leukaemia.
miRNA network regulates SETD2 in in colorectal metastasis tissues.
Huntington's disease (HD), a neurodegenerative disorder characterized by loss of striatal neurons, is caused by an expansion of a polyglutamine tract in the HD protein huntingtin. This gene encodes a protein belonging to a class of huntingtin interacting proteins characterized by WW motifs. This protein is a histone methyltransferase that is specific for lysine-36 of histone H3, and methylation of this residue is associated with active chromatin. This protein also contains a novel transcriptional activation domain and has been found associated with hyperphosphorylated RNA polymerase II.
histone-lysine N-methyltransferase SETD2
, kinesin family member 9
, huntingtin interacting protein 1
, huntingtin yeast partner B
, huntingtin-interacting protein B
, lysine N-methyltransferase 3A