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Chloride
Channels (CLC1-7, CLC-K1/K2) Antibodies
Chloride is a critical component of all living cells. It is also the single most
dominant diffusible anion inside of most cells - the others are mostly
impermeable organic anions. Since cytoplasmic electroneutrality is maintained
under normal physiological environment, changes in cellular chloride level is
accompanied by total cell solute content. Because of high water permeability of
cell membranes, changes in cell solute content are accompanied by changes in
cellular volume. Voltage-gated chloride channels regulate cellular traffic of
chloride ion. The chloride channels (CIC or CLC) perform several functions
including the regulation of cell volume, membrane potential stabilization,
signal transduction, and transepithelial transport. Mutations in CIC genes have
been linked with several human diseases including myotonias (Thomsen's disease),
cystic fibrosis, Bartters syndrome type III, Dent's disease, and X-linked
recessive nephrolithiasis.
Since the cloning of first member of CLC from Torpedo electric organ (CLC-0),
many mammalian homolgs have been identified. In mammals, CLC proteins form a
superfamily of at least 9 different genes (CLC1-7 also known as CLCN1-7 and
CLK1-2 or CLCKa and CLCKb). Additional forms of these proteins are obtained by
alternative splicing. A detailed sequence comparison of CLC has revealed three
closely related groups: One group contains CLC-1, CLC-2, and the renal CLC-K1
and CLC-K2; a Second group comprises of CLC-3, CLC-4, and CLC-5; The third group
has CLC-6 and CLC-7. All CLC proteins (~700-1000 aa) are predicted to contain 10
(possibly 12) transmembrane domains with intracellular N and C-termini. Except
CLC-1 and CLC-K1/K2 that are specific for kidney, most other CLC are widely
distributed in various tissues.
CLC-1 has been linked with myotonia congenita, an unusual syndrome associated w
ith muscular stiffness caused by delayed relaxation of muscle following
voluntary contractions. Bartter's syndrome, a rare disorder associated with
renal salt wasting and hypokalemic alkalosis, has mutation in CLC-K2. Mutations
or deletions in CLC-5 have been linked with Dent's diseases (excessive urinary
calcium, urinary low mol wt proteinuria, and calcium kidney stone), and four
related X-linked syndromes of hypercalciuric nephrolithiasis.
ADI has produced highly specific rabbit antibodies to CLC1-7, and CLC-K1/K2
using peptide sequences specific to each CLCs. These antibodies should be useful
in studying various CLCs.
|
Items |
Antigen
peptide location |
Antibody
Host |
Expected
Ab Crossreactivity |
Antiserum
Cat #
(100 ul) |
Aff.
Pure IgG
Cat #
(100 ug) |
* Control
Peptide Cat#
(100 ug) |
|
CLC1 |
r, 18 aa ~CT |
Rb |
m, r, h |
CLC11-S |
CLC11-A |
CLC11-P |
|
CLC1 |
r, 19 aa ~NT |
Rb |
m, r, h |
CLC12-S |
CLC12-A |
CLC12-P |
|
CLC2 |
r, 22 aa ~CT |
Rb |
r, h, m, rb |
CLC21-S |
CLC21-A |
CLC21-P |
|
CLC3 |
r, 18 aa ~CT |
Rb |
m, r, h, f, c |
CLC31-S |
CLC31-A |
CLC31-P |
|
CLC4 |
r, 13 aa ~CT |
Rb |
m, r, h |
CLC41-S |
CLC41-A |
CLC41-P |
|
CLC5
|
r, 13 aa ~CT
|
Rb
|
m, r, h
|
CLC51-S
|
CLC51-A
|
CLC51-P
|
|
CLC6
|
r, 19 aa ~CT
|
Rb
|
m, h
|
CLC61-S
|
CLC61-A
|
CLC61-P
|
|
CLC7
ab # 1
|
r, 23 aa ~CT
|
Rb
|
r, m, h
|
CLC71-S
|
CLC71-A
|
CLC71-P
|
|
CLC7 ab # 2
|
r, 15 aa ~NT
CP Domain
|
Rb, poly
|
r, m, h
|
CLC72-S
|
CLC72-A
|
CLC72-P
|
|
CLCK1/K2
|
r, 17 aa ~CT
|
Rb
|
r, h
|
CLCK11-S
|
CLCK11-A
|
CLCK11-P
|
|
Barttin
|
h, 16-aa ~NT
CP domain
|
Rb
|
r, h
|
BRTN11-S
|
BRTN11-A
|
BRTN11
|
|
Control Rabbit IgG |
For
use in ELISA, Western, Immunohisto. |
20009-1 (1 mg) |
m=mouse; r=rat; h=human; c=chicken; f=frog; ~CT or
~NT=near C or N-terminus.
"Neat Antisera"
are the unpurified antiserum and it is suitable for
ELISA and Western.
"Affinity pure"
antibodies have been over the
antigen-affinity column and recommended for
immunohistochemical applications.
"Control peptides"
can not be used for Western as they are very short
peptides. They are intended for ELISA or antibody
competition studies.
All
Products are for in vitro research use only.
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