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CSRP3 encodes a member of the CSRP family of LIM domain proteins, which may be involved in regulatory processes important for development and cellular differentiation. Additionally we are shipping CSRP3 Proteins (8) and CSRP3 Kits (2) and many more products for this protein.
Showing 10 out of 82 products:
Human Polyclonal CSRP3 Primary Antibody for ELISA, ICC - ABIN451632
Zheng, Wen, Han: hhLIM is a novel F-actin binding protein involved in actin cytoskeleton remodeling. in The FEBS journal 2008
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Cow (Bovine) Polyclonal CSRP3 Primary Antibody for WB - ABIN2778310
Geier, Perrot, Ozcelik, Binner, Counsell, Hoffmann, Pilz, Martiniak, Gehmlich, van der Ven, Fürst, Vornwald, von Hodenberg, Nürnberg, Scheffold, Dietz, Osterziel: Mutations in the human muscle LIM protein gene in families with hypertrophic cardiomyopathy. in Circulation 2003
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Previous results along with the newly identified homozygous CSRP3 truncating variants in two unrelated hypertrophic cardiomyopathy (HCM) patients suggest that the association of CSRP3 as a validated HCM-causing gene require additional studies and those CSRP3 variants could result in HCM with an autosomal recessive inheritance rather than with an autosomal dominant transmission as usually reported on HCM.
MLP contributes to the maintenance of cardiomyocyte cytoarchitecture by a mechanism involving its self-association and actin filament cross-linking.
study reports the discovery of an alternative splice variant of muscle lim protein encoded by the CSRP3 gene, designated as MLP-b, showing distinct expression in neuromuscular disease and direct roles in actin dynamics and muscle differentiation
KLF5 reverses hhLIM function from anti-proliferation to pro-proliferation through its interaction with hhLIM on the cyclin E promoter.
The CSRP3-W4R mutation causes cardiomyopathy and heart failure in patients and engineered knock-in animals.
CSRP3 is involved in cardiac mechanosensory processes, is localized to the sarcomeric Z-disc and human mutations cause cardiomyopathy(DCM)and heart failure.
Mutations in the CRP3/MLP gene can cause hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM).
CSRP3, MUSTN1, SIX1, and FBXO32 expression changes in response to lengthening and shortening contractions in human muscle
A myocardial actin-binding protein that increases actin cytoskeleton stability by promoting bundling of actin filaments.
These findings suggest that hhLIM is a typical LIM family member with powerful transcription activation.
Study used linkage analysis and identified a CSRP3 missense mutation in a large German family affected by hypertrophic cardiomyopathy.
CSRP3 mutation was found involved in hypertrophic cardiomyopathy.
The structure of both LIM domains of human MLP by nuclear magnetic resonance spectroscopy.
CRP3/MLP is primarily expressed in arterial smooth muscle cells and that stretch is the main stimulus for CRP3/MLP induction in veins exposed to arterial haemodynamic conditions.
Complete chemical shift assignment was achieved for the first LIM domain and for most of the second domain, the N-terminal and C-terminal linker and part of the intervening linker.
MLP binds directly to CFL2 in human cardiac and skeletal muscles.
Cardiac overexpression of muscle LIM protein does not modulate the heart's response to various forms of pathological stress.
Loss of MLP leads to dilated cardiomyopathy and hearts of surviving MLP knockout mice show transient changes of intracellular calcium handling.
Report a common MLP (muscle LIM protein) variant associated with a hypertrophic cardiomyopathy and heart failure phenotype, and skeletal muscle pathology.
Reduced MLP-calcineurin signaling predisposes to adverse remodeling after myocardial infarct.
results indicate that the progression to heart failure in the MLPKO model may be driven by diastolic myocardial dysfunction and abnormal passive properties rather than systolic dysfunction
This detailed physiological characterization during a phase of rapid anatomical remodeling suggests that systolic function in the MLP(-/-) mice may temporarily improve as a result of alterations in chamber compliance, which are mediated by dilatation.
Mice with knockout of muscle-LIM protein exhibit prolongation of atrial and ventricular conduction and an increased ventricular vulnerability.
data support the high potential of the CSRP3 as a marker gene for the improvement of growth performance and carcass traits in selection programs
CSRP3 coding gene from porcine muscle was isolated and characterized and Phylogenic analyses demonstrated that CSRP3 diverged first and is distinguished from two other members, CSRP1 and CSRP2.
is only expressed in the differentiated heart during early development and is expressed in a subset of other striated muscles during later stages
This gene encodes a member of the CSRP family of LIM domain proteins, which may be involved in regulatory processes important for development and cellular differentiation. The LIM/double zinc-finger motif found in this protein is found in a group of proteins with critical functions in gene regulation, cell growth, and somatic differentiation. Mutations in this gene are thought to cause heritable forms of hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) in humans. Alternatively spliced transcript variants with different 5' UTR, but encoding the same protein, have been found for this gene.
LIM domain only 4
, cardiac LIM domain protein
, cysteine and glycine-rich protein 3
, muscle LIM protein
, LIM domain protein, cardiac
, cardiac LIM protein
, cysteine-rich protein 3
, cysteine- and glycine-rich protein 3
, Cysteine and glycine-rich protein 3
, Muscle LIM protein
, cysteine and glycine-rich protein 3 (cardiac LIM protein)