PA5-16446

antibody from Invitrogen Antibodies

Targeting: MKI67 MIB-1, PPP1R105

Provider product page for PA5-16446

Immunocytochemistry

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [24]
Comments [0]
Validations
Immunocytochemistry [1]
Immunohistochemistry [3]
Other assay [8]

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Product number: PA5-16446 - Provider product page
Provider: Invitrogen Antibodies
Product name: Ki-67 Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Description: PA5-16446 targets Ki-67 in IHC (P) applications and shows reactivity with Rat and Human samples.
Concentration: 1 mg/mL

MKI67 protein structure - PA5-16446 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Formalin-fixed, paraffin-embedded human tonsil stained with Ki67 antibody using peroxidase-conjugate and AEC chromogen. Note nuclear staining of proliferating cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunohistochemistry analysis of Ki-67 showing staining in the nucleus of paraffin-embedded human breast tissue (right) compared to a negative control without primary antibody (left). To expose target proteins, antigen retrieval was performed using 10mM sodium citrate (pH 6.0), microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with a Ki-67 Rabbit Polyclonal Antibody (Product # PA5-16446) diluted in 3% BSA-PBS at a dilution of 1:20 for 1 hour at 37°C in a humidified chamber. Tissues were washed extensively in PBST and detection was performed using an HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunohistochemistry analysis of Ki-67 showing staining in the nucleus of paraffin-embedded human tonsil tissue (right) compared to a negative control without primary antibody (left). To expose target proteins, antigen retrieval was performed using 10mM sodium citrate (pH 6.0), microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with a Ki-67 Rabbit Polyclonal Antibody (Product # PA5-16446) diluted in 3% BSA-PBS at a dilution of 1:20 for 1 hour at 37°C in a humidified chamber. Tissues were washed extensively in PBST and detection was performed using an HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4. Knockdown of Ki-67 expression in HEp2 cells at 24 h after siRNA transfection. (A) Ki-67 mRNA levels were determined by RT-qPCR. Relative fold induction for Ki-67 mRNA (means +- SD) in the mock- and Ki-67 siRNA-transfected HEp2 cells is presented relative to the expression in the parental HEp2 cells (*P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 Cell proliferation starting from day-9 following oncogenic KRAS activation. ( A ) Nuclear Ki-67-positive cells increased mainly at the ductal cells starting from day-9 post KRAS G12V induction. Scale bars: 250 mum; inset : 200X; A: acini; D: duct; black arrow: nuclear Ki-67-positive ductal cell; red arrow: nuclear Ki-67-positive fibroblast; red arrowhead: blood vessel. The relative fold change in the nuclear Ki-67-positive staining with the level in the SMGs of LGL-KRas G12V ;Ela-CreERT mice prior to Tam-feeding (Ctrl) set as 1. Results are shown as mean +- S.D. enumerated from 6 randomly selected non-overlapping fields (10X) by Image-Pro Premier 9.0; * p < 0.05, ** p < 0.01. ( B ) Elastase I accumulation in the SMG ductal cells of LGL-KRas G12V ;Ela-CreERT mice decreased during the course of tumorigenesis ( left panels ). Panel d (enlarged from boxed region in panel b ): elastase I staining was lost in a GCT (shown by dotted line, panel d ) near a dyad structure of a striated duct (blue arrow) and a blood vessel (red arrow); residual elastase I staining was visualized in some GCTs (label with G). Scale bar: 100 mum ( panels a-c :); 100 mum ( panel d , enlarged from b ). The relative fold change in the elastase I-positive staining ( right panel ). Quantitative analyses of elastase I-positive staining with level at control SMGs set as 1. Results are shown as mean +- S.D. enumerated from 5 randomly selected non-overlapping fields (10X) by Image-Pro Premier 9.0; ** p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 1. Immunohistochemical staining of Ki-67 protein of laryngeal squamous carcinoma tissues and the corresponding non-cancerous tissues (magnification, x200). (A) Strong immunostaining for Ki-67 protein in laryngeal squamous carcinoma tissue. (B) Ki-67 protein expression is absent in non-cancerous laryngeal tissue.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 1 Early sagittal fibers on coronal Nissl ( a, b ) and immunostained histological sections ( c - h ) through the occipital ( a, b ) and midlateral levels ( c - h ) of the brain at 9 ( a, b ) and 11 ( c - h ) PCW. The rectangle in 'a', 'c', 'e', and 'g' are shown at higher magnifications in 'b', 'd', 'f', and 'h' respectively. The intermediate zone (IZ) contains large fiber bundles ( b asterix), running in a sagittal direction separated by groups of migratory neurons ( b arrowheads). Coronal sections through the brain at 11 PCW showed SNAP25 immuno-positivity to sagittal fibers in the IZ ( c, d ). Some fibers originating from the thalamus showed radial orientation before attaining sagittal orientation ( d arrowhead). The IZ is well delineated from the presubplate ( d asterisk) and ventricular zone (VZ), but intermingles with the subventricular zone (SVZ). Staining of the same brain (11 PCW) for SOX2 ( e, f ) and Ki67 ( g, h ) showing a homogenous VZ but dispersed SVZ. ( CP cortical plate; MZ marginal zone). Scale bar = 100 um ( b ); 200 um ( d, f )

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 12 Maturation of the occipital sagittal strata (SS) on coronal plane T2 MR images ( a, h ), and corresponding histological preparations from newborn ( b - g ) and preterm ( i - n ) brains. The rectangle in b, d, f, i, k , and m are shown at higher magnification in c, e, g, j, l , and n , respectively. Comparison of MRI scans through the occipital lobe in a newborn infant ( a ) and a premature infant scanned at term equivalent age ( h ) suggested a slight difference in visibility and delineation of the sagittal strata ( a , h arrow) fashioned as a visible ""triplet structure"". Histological sections of Nissl-stained ( b, c; i, j ) preparations, sections immunostained for the proliferative marker Ki67 ( d, e; k, l ) and myelin basic protein SMI99 ( f, g; m, n ) indicated that different underlying factors contribute to the MRI ""triplet"" appearance in preterm and term periods. The differential prominence of cell and fiber layers, and the differential appearance of proliferative cells and myelination of the visual pathway at preterm and term determined the structure of the occipital SS. The less visible ""triplet structure"" in a preterm infant at TEA ( h ) was probably due to the disappearance of the transient proliferative cell band (arrow, l ; please, see MRI scan of preterm brain scanned soon after birth on Fig. 9 ) and impaired myelination ( n arrow). In the newborn brain, histological coronal sections through the occipital lobe ( f, g ), at the level of the

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 8 Laminar organization of the sagittal strata during the early preterm period. Coronal Nissl-stained frozen section ( a, b ) through the parietooccipital portion of the brain at 26 PCW showing a similar laminar organization as seen in the previous phases (see Fig. 5 ). The internal sagittal stratum (ISS) is densely cellular ( b number 5), and this stratum may be partially defined on both AChE-stained and unstained portion ( d ) on section of the brain at the same age. At this age, both cellular (O)SVZ and former fibrillar intermediate zone now are incorporated in multilaminar axonal-cellular compartment (MACC). Rectangles in a, c, e, g , and i are shown at higher magnifications in b, d, f, h , and j , respectively. Sublamination of the sagittal fiber strata and related cell layers were also visible on horizontal histological sections of brain at 24.5 PCW when immunostained for vimentin ( e, f ), GFAP ( g, h ), and Ki67 ( i, j ). Numbers (1-8) used to mark the laminas are explained in detail in Fig. 5 . Immunostaining for glial markers ( e - h ) showed that the radial glia transverses the radial-sagittal strata and subplate (SP) to reach the cortical plate (CP). Immunostaining for proliferative markers ( i, j ) showed proliferative activity in cellular-fibrillar layers, except in the compact periventricular (callosal) system. The two proliferative cell layers ( b between arrows) were not a constant finding on Nissl-stained preparations of the occipital lobe (see