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anti-Human KALRN Antibodies:
anti-Mouse (Murine) KALRN Antibodies:
anti-Rat (Rattus) KALRN Antibodies:
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Human Polyclonal KALRN Primary Antibody for IHC (p), IHC - ABIN188543
Colomer, Engelender, Sharp, Duan, Cooper, Lanahan, Lyford, Worley, Ross: Huntingtin-associated protein 1 (HAP1) binds to a Trio-like polypeptide, with a rac1 guanine nucleotide exchange factor domain. in Human molecular genetics 1998
Cow (Bovine) Polyclonal KALRN Primary Antibody for ELISA - ABIN451733
Xie, Srivastava, Photowala, Kai, Cahill, Woolfrey, Shum, Surmeier, Penzes: Kalirin-7 controls activity-dependent structural and functional plasticity of dendritic spines. in Neuron 2007
The GG genotype and G allele of SNP rs7620580 were associated with a risk for ischemic stroke with an adjusted OR of 3.195 and an OR of 1.446, respectively. Haplotype analysis revealed that A-T-G,G-T-A, and A-T-A haplotypes were associated with ischemic stroke. Our results provide evidence that kalirin gene variations were associated with ischemic stroke in the Chinese Han population.
DNA sequencing provided evidence linking KALRN to monogenic intellectual disability in two patients.
Data suggest protein levels of kalirin and CHD7 (show CHD7 Antibodies) in circulating extracellular vesicles (EVs) as endothelial dysfunction markers to monitor vascular condition in hypertensive patients with albuminuria.
GG genotype and the G allele of the rs9289231 polymorphism of KALRN and the rs224766 polymorphism of ADIPOQ genes may be considered genetic risk factors for Iranian type 2 diabetic patients with coronary artery disease.
4 KALRN gene SNPs were studied in Han ischemic stroke patients. rs11712619 seemed associated with lacunar stroke until risk factors were considered. re6438833 was significantly associated with ischemic and lacunar stroke.
consider the GG genotype and the G allele of rs9289231 polymorphism of KALRN to be genetic risk factors for CAD (show CAD Antibodies) in an Iranian population, especially in early-stage atherosclerotic vascular disease
A sequence variant in human KALRN impairs protein ability to activate Rac1 and coincides with reduced cortical thickness.
The kalirin expression were reduced in Alzheimer disease with psychosis.
The age-at-onset of Huntington disease (HD (show HTT Antibodies)) is not associated with eleven SNPs, including SNP rs10934657 in the kalirin gene in 680 European HD patients.
Neuronal guanine nucleotide exchange factor (show NGEF Antibodies) (GEF (show SLC2A4RG Antibodies)) kalirin is emerging as a key regulator of structural and functional plasticity at dendritic spines.
Kalirin reduction in APPswe/PSEN1dE9 mice significantly attenuated psychosis-associated behavior at 12 months of age without changing spatial memory performance.
Kalirin-7 plays a prominent role in nociceptive sensitization via activity-dependent modulation of spinal synapses.
lack of Kalrn expression in POMC (show POMC Antibodies) cells closely mimicked the effects of global Kalrn knockout on anxiety-like behavior and passive avoidance conditioning
Kalirin may play a role in paracrine and/or endocrine signaling events that control skeletal bone remodeling and the maintenance of bone mass.
Many of the widespread and diverse deficits observed both within and outside of the nervous system when expression of Kalrn is eliminated may reflect its role in secretory granule function and its expression outside of the nervous system.
Kalirin functions as a guanine nucleotide exchange factor for Rac1 in smooth muscle cells, promoting migration and proliferation.
Kalirin-7 is an selectively essential modulator of NMDA receptor-dependent synaptic plasticity in the hippocampus.
Identification of kalirin-7 as a potential post-synaptic density signaling hub
This study demonstrated a novel and functionally important interaction between the NR2B (show GRIN2B Antibodies) subunit of the NMDA receptor and Kalirin, proteins known to be essential for normal synaptic plasticity.
These data suggest that hippocampal structure and function are more resilient to the complete loss of kalirin, and reveal impairments in fear learning.
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 that interacts with the huntingtin-associated protein 1, which is a huntingtin binding protein that may function in vesicle trafficking. Alternatively spliced transcript variants encoding different isoforms have been described.
SEC14 domain and spectrin repeat-containing protein 1
, protein Solo
, kalirin, RhoGEF kinase
, huntingtin-associated protein interacting protein (duo)
, serine/threonine kinase with Dbl- and pleckstrin homology domains
, serine/threonine-protein kinase with Dbl- and pleckstrin homology domain
, protein Duo
, serine/threonine kinase with Dbl- and pleckstrin homology domain
, PAM COOH-terminal interactor protein 10
, cyclin B1
, huntingtin-associated protein-interacting protein